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Renal Final > Regulation of K, Ca, PO4, Mg > Flashcards

Regulation of K, Ca, PO4, Mg Flashcards

1
Q

What are two hallmark signs of hyperaldostronism?

A

Hypokalemia and metabolic alkalosis.

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2
Q

In a patient with hyperaldostronism, osmolarity doesn’t change, why?

A

With aldosterone, patient would reabsorb both Na and water proportionately, thus not affecting osmolarity.

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3
Q

In a patient with HYPOatdostronism, how does osmolarity change?

A

Osmolarity decreases. Without ADH, the body is not able to retain Na and so the patient will present with hyponatremia.

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4
Q

What happens to the resting membrane potential of a patient with hypokalemia?

A

The membrane potential increases and thus takes longer for a AP to occur. Patient would present with muscle weakness.

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5
Q

Normally, ECF concentration of K is 65 mmole. There was a disturbance where K had to move into cells. How will patient’s electrolyte balance, acid-base balance change?

A

patient will become hypokalmic and is at risk of acidosis.

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6
Q

Patients with acidosis are at risk of _?

A

hyperkalemia.

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7
Q

What are some factors that can cause K to move out of the cell and into the blood?

A
  1. Acidemia
  2. hyperosmolarity
  3. Ischemia (cell damage)
  4. heavy exercise.
  5. Hypokelemia
  6. a-adrenergic agonist
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8
Q

What are some factors that can cause K to move into the cell and out of the blood?

A
  1. Hyperkalemia
  2. Alkalemia
  3. b-adrenergic agonist
  4. insulin
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9
Q

Diabetics are at risk hyperkalemia, why?

A

Insulin is a way to move K out of the blood and into the cell. If the patient is insulin deficient or insulin does not work, the patient is not able to move K out of the blood when there’s too much K in the blood.

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10
Q

What percentage of K is reabsorbed in the PCT? TAL?

A

67% in the PCT

20% in TAL

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11
Q

How does K get reabsorbed in the TAL?

A

Via Na, K, 2Cl cotransporter

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12
Q

What are five factors that which affect K secretion in the collecting duct?

A
  1. EC K concentration
  2. Na reabsorption: negative luminal voltage attracts K via leak channels
  3. Luminal fluid flow rate
  4. EC pH: K and H exchange across cell membranes.
  5. Aldosterone: stimulates K secretion in collecting duct to maintain electroneutrality when na is reabsorbed.
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13
Q

Normally, excess K is excreted from the body without causing much problem. How is this balance changed in a person who is on a loop diuretic?

A

Patient will be at risk for developing hypokalemia and thus may require K supplements.

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14
Q

How sodium diet can cause _ 1_ K secretion, and thus may cause 2.

A
  1. less

2. Hyperkalemia.

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15
Q

How can you increase Na delivery to late distal tubule and collecting duct?

A

By using a diuretic.

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16
Q

One way to treat hyperkalemia is to secrete it in the DCT/Collecting duct. How can this be accomplished?

A

By using a diuretic which increasing downstream delivery of Na to the distal tubules/collecting ducts. This results in increased Na reabsorption and K secretion.

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17
Q

In the collecting duct principal cells can exchange which ions to increase K secretion and where (apical vs basolateral) is this exchanger located?

A

Na/K exchanger on the apical side.

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18
Q

Principal cells is also able to decrease K secretion by what mechanism?

A

Increased H causes H/K exchange which lowers IC K concentration and thus decreases K secretion.

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19
Q

How does K secretion change in an acidodic pt vs an alkolatic patient?

A

In acidodic pt K secretion is decreased (body is trying to secrete H instead)
In an alkalatic pt, K secretion increases.

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20
Q

What effect does increased plasma [K] have on aldosterone secretion?

A

increases aldosterone secretion

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21
Q

What is the mechanism by which aldosterone stimulates K secretion by the principal cells?

A

Aldosterone translocates to the nucleus and causes transcription of new Na/K ATPase which are then inserted at the basolateral membrane and increases their activity. It also transcribes new potassium channels and inserts them on the luminal side of the membrane for K to get secreted.

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22
Q

True or false : Aldosterone is more sensitive to K levels than it is to stimulation by Ang II

A

True.

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23
Q

What is Conn’s disease?

A

Primary hyperaldosteronism. Tumor on adrenal cortex causing inappropriate amount of aldoserone secretion.

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24
Q

What is the consequence of hyperaldosteronism?

A

Hypokalemia

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25
Q

What is Addison’s disease?

A

Hypoaldosteronism. Destruction of adrenals (maybe due to autoimnune process)–> aldosterone isn’t secreted.

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26
Q

What electrolyte imbalances are consequence of addison’s disease?

A

hyperkalemia and hyponatremia

27
Q

What is ∂-intercalated cells responsible for?

A

reabsorption of K and H secretion.

28
Q

What transporters/pumps can you find on ∂-intercalated cells and what side are they located?

A
  1. H/K ATPase on the luminal side which pumps out H and takes in K.
  2. H ATPase on the luminal side which functions in acid-base balance
29
Q

In hyperaldosteronism, what is the net movement of K and H

A

Net K and H secretion of

30
Q

During acidosis what is the net movement of H and K?

A

K reabsorption, H secretion

31
Q

During alkalosis what is the net movement of H and K

A

H reabsorption, K secretion

32
Q

During hyperkalemia what is the net movement of H and K?

A

H reabsorption and K secretion

33
Q

During hypokalemia what is the net movement of Ha nd K

A

K reabsorption and H secretion

34
Q

What kind of diuretic acts on the Proximal tubule and what is an example of such?

A
  1. Osmotic diuretics such as mannitol. Inhibits reabsorption of water and secondarily Na.
  2. Carbonic anhydrase inhibitor (e.g. acetazolamide): inhibits NaHCO3 reabsorption.
35
Q

What is an example of a loop diuretic and how does it work?

A

Loop diuretic works at the TAL to inhibit Na/K/2Cl cotransporter and thus eliminate’s half of the kidney’s ability to concentrate urine. Lessens water reabsorption in descending limb of henle, medullary collecting duct.
Examples: Furosamide (lasix), bumetenide (bumex), ethacynic acid

36
Q

What kind of diuretic acts in the DCT and how does it work? Give an example of this type.

A

Thiazide diuretics. Inhibits Na/Cl cotransporter. Increases Na, Cl, and K excretion and decrease Ca excretion. Example: hydroclorothiazide.

37
Q

What kind of diuretic works at the collecting duct and how does it work?

A

Potassium sparing diuretics. Inhibits Na reabsorption and K secretion. Example: amiloride, triamtrene, spironolactone (aldosterone antagonist)

38
Q

How does hypocalcemia affect muscle?

A

produces hypocalcemic tetany.

39
Q

What % of total Ca is biologically active?

A

About 55% or about 1.2 mM.

40
Q

What is the Ca concentration in Bowman’s capsule? why?

A

Only half of total Ca can be filtered because the other half is bound to protein which cannot get filtered.

41
Q

What happens to plasma Ca levels in a patient with acidemia?

A

Ca levels increases since the increased H+ in the blood completes with binding site on proteins.

42
Q

An alkalotic patient is at risk for hypocalcemia, why?

A

With reduced H+ in the blood, Ca can freely remain bound to plasma proteins and thus decreasing the free Ca levels in plasma.

43
Q

How does the brain respond to decreased plasma Ca levels?

A

Signals PT to release PTH.

44
Q

What effect does PTH have on the kidney?

A

Hydroxylates Vit D to Calcitriol (Vit D3)

45
Q

How does Calcitriol increase Ca levels?

A
  1. Causes GI to reabsorp more Ca from diet.

2. Acts on bone to promote osteoclastic activity.

46
Q

Where is most of the Ca reabsorbed and what is the mechanism?

A

PCT (70%).

Mechanism: 1. paracellular; 2. Transcellular via the 3Na/Ca exchanger on the basolateral membrane.

47
Q

What percentage of Ca is reabsorbed in the TAL and what is it’s MOA?

A

20% is reabsorbed via paracellular reabsorption. This is possible due to the ~6mV transepithelial potential.

48
Q

What gives the TAL it’s +6mV?

A

In the TAL Na/Cl reabsorbs Na and Cl. With no Cl- in the lumen, raises the positivity of the lumen.

49
Q

What other ions are able to get reabsorbed paracellularly at the TAL along with Ca?

A

K, Mg, NH4, Na

50
Q

What type of reabsorption of Ca is possible in the DCT? What % is reabsorbed here?

A

Transcellular. 8%

51
Q

What controls Ca reabsorption in the DCT/

A

PTH

52
Q

How does a loop diuretic affect Ca reabsorption?

A

Reabsorption is decreased because a loop diuretic abolishes the +6mV that is needed for reabsorption to occur in the TAL.

53
Q

What role does vitamin D play in DCT reabsorption of Ca?

A

vitamin D activates Ca channels in the tubular cell. Ca enters the cell and binds calbindin and is reabsorbed via Ca ATPase and 1Ca/3Na exchanger at the basolateral side.

54
Q

With a thiazide, Ca reabsorption is enhanced, why?

A

Thiazides inhibit he Na/Cl symport in the early DCT, thus causing a decrease in IC Na. This, in turn, enchces the activity of the Na/Ca2 exchanger, creating an increased driving for Ca 2+ reabsorption through the epithelial Ca2 channels.

55
Q

As plasma Ca increases, what hormone levels are increased/decreased?

A

Calcitonin increases

PTH decrease

56
Q

As plasma Ca goes down, what hormone level is increaed?

A

PTH

57
Q

In some patients with kidney disease, you’ll also see bone resorption leading to fibrotic and diseased bone. What can cause this?

A

Kidney regulates Ca level by PTH which hydroxylates Vit D to calcitriol. With diminished kidney function, you will not be able to regulate convert Vit D and thus cannot produce calcitriol. As a compensatory mechanism, PTH will signal bones to increase resorption. this increased bone resorption will make the bone fibrotic and diseased.

58
Q

What % of phosphate is reabsorbed in the PCT? in DCT?

A

80% in PCT. 10% in DCT. 10% is excreted.

59
Q

What is the mechanism by which phosphate is reabsorbed?

A

Na/K ATpase drives the force to create gradient. From the tubular fluid, 2Na/Pi cotransporter brings phosphate into the cell. At the basolateral side, Pi leveas the cell and enters blood via Pi/A- antiporter.

60
Q

Does PTH increase or decrease Pi reabsorption? why?

A

decrease. PTH causes Ca reabsorption which uses the same transporter as Pi. PTH inhibits Pi reabsorption.

61
Q

What are three ways Mg is carried in plasma?

A
  1. 60% in free mg - biologically active
  2. 20% complexed with inorganic, small organic anions
  3. 20% bound to plasma proteins
62
Q

How is bulk of the Mg reabsorbed and where?

A

Via paracellular reabsorption in the TAL.

63
Q

What drives Mg reabsorption in TAL?

A

Cl reabsorption via the Na/K, 2Cl cotransporter, making the tubular fluid +6mV.

Renal Final (7 decks)

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