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FHB - Pulmonary & Renal - Exam 2 > Renal- Regulation of Electrolytes - Lecture 9 > Flashcards

Renal- Regulation of Electrolytes - Lecture 9 Flashcards

1
Q

Why is the regulation of K+ within narrow limit so crucial to life?

A
  1. Regulates Cell volume
  2. Intracellular pH
  3. Synthesis of DNA and protein
  4. RMP
  5. Cardiac and neuromuscular activity
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2
Q

Describe the following in terms of intake & output:

  1. Positive K balance
  2. Negative balance

Which is hyperkalemia & which is hypokalemia?

A
  1. Positive K: intake > output (hyperkalemia)

2. Negative K: intake < output (hypokalemia)

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3
Q

An change in which hormones stimulates the movement of K INTO cells and decreases plasma volumes?

Does the concentration of the hormones have to increase or decrease for the aforementioned changes to occur?

A
  1. Insulin
  2. Epinephrine
  3. Aldosterone
  • all have to increase; stimulate K moving into the cell (via na/k ATPase for example)
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4
Q

When is an individual in K balance? What is K excretion regulated by? (3)

A

When K intake = K output (plus output by the gastrointestinal tract)

  • K excretion is regulated by
    1. ADH
    2. Aldosterone
    3. Plasma K
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5
Q

What are 3 mechanisms in which K+ is released from cells ?

Briefly describe how these changes occur.

A
  1. Epinephrine - exercise & alpha 1 receptor stimulation causes K+ to be released (action potentials) –> vasoconstriction
  2. Cell Lysis (surgery, burns)
  3. Hyperosmolality
    - cells shrink, K concentration inside the cell increases, this increases the driving force on K to LEAVE the cell
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6
Q

What are 5 mechanisms in which K is taken UP INTO THE CELL?

A
  1. Na/K ATPase
    - increase in extracellular K stimulates Na/K ATPase uptake of K into cells
  2. Insulin
    - shifts K into cells post prandial
  3. Epinephrine
    - stimulation of B2 receptors
  4. Aldosterone
    - stimulation of Na/K ATPase
    - increased urinary excretion of K
  5. HYPOSMOLALITY
    - cells swell–> [K] inside the cell is diluted –> increases the driving force of moving K INSIDE the cell
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7
Q

What is the normal excretion & reabsorption of K+ by the kidney?

How do these values changed with increased/decreased dietary K+ intake?

A

Excretion - 15%
Reabsorption - 85%

Increase dietary K: enhanced K+ EXCRETION (to 80%)

Decrease Dietary K: enhanced K+ REABSORPTION (to 99%)

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8
Q

What are the 3 principal factors that regulate the rate of K+ secretion by DT and CD?

A
  1. Na/K ATPase pump
  2. tubular cell to tubular lumen electrochemical gradient (-40mV)
  3. K+ permeability of apical membrane
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9
Q

Describe the mechanism of increased K outside the cell & aldosterone in regulating K+ secretion.

A
  1. Increased [K+] outside–> stimulates Na/K -ATPase –> increases [K]inside –> increases apical membrane permeability to K+ –> increases K+ secretion
  2. Increased [K+] outside –> stimulates aldosterone –> stimulates K+ secretion
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10
Q

In response to potassium depletion, which parts of the nephron decrease their secretion of K+? How much of the filtered load of K+ is excreted under these conditions?

How much is excreted under normal/high K+ conditions?

A
  1. Distal Tubule
  2. Cortical Collecting Duct
  3. Medullary Collecting Duct

1% under low K+

15%-85% under normal/high K+

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11
Q

What hormones alter K+ secreting?

A
  1. Aldosterone –> stimulate Na/K ATPase (increase K inside the cell) –> Increase K secretion
  2. Glucocorticoids –> increase K+ secretion (indirect via GFR increases!)
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12
Q

ADH has an affect on K+ secretion. True or false.

A

FALSE no net affect on K+

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13
Q

What 3 factors alter K+ secretion?

A
  1. Hormones (Aldosterone & Glucorticoids)
  2. Tubular Flow Rate –> increase flow = increased secretion
  3. Dietary Intake –> high K+ diet = high secretion
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14
Q

If distal tubule flow rate increases (diuresis) how is K+ secretion & ADH changed?

A

Increased flow rate results in increased K+ secretion and decreased ADH

  • this results in tubular negativity
  • which finally results in decreased K+ secretion (or K+ balance maintained)
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15
Q

If one’s diet is low in K+, how is secretion and excretion of K+ changed?

A

Decreased K+ secretion & excretion (K+conservation)

  • if you increase K+ diet = “K+ spilling”
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16
Q

What are the reasons that ADH has no affect on K+ secretion?

A

Increased ADH results in:

  1. Increased electrochemical for K+ across apical membrane
  2. Increase permeability of K+ on apical membrane

BUT!! It is opposed by the DECREASED FLOW RATE that results from an increase in ADH!

therefore the net K+ secretion is not affected by ADH!

17
Q

How does ACUTE metabolic ACIDOSIS affect K+ secretion & excretion? Why?

A
  1. Decreases K+ permeability of apical membrane in DT and CD

this results in decreased K+ secretion and excretion!!!

A) inhibits Na/K ATPase pumps which results in increased plasma K and cells do not secrete the excess plasma K into the tubule since the increased H+ concentration also affects the pumps on the lumenal membrane

B) Decreases K+ permeability

18
Q

How does CHRONIC metabolic acidosis affect K+ excretion and secretion?

A

Increased [K+ out/H+ in ] exchange –> this increases plasma K+

  • increases in K+ plasma concentration activates aldosterone system
  • increased K+ permeability of apical membrane in DT and CD
  • increased secretion and excretion!!!
19
Q

How do diuretics affect K+:

Which are K+ sparing and which are K+ wasting?

  1. Furosemide
  2. Acetazolamide
  3. Mannitol
  4. Spironolactone
  5. Amiloride
A

K+ Wasting: (FAM)

  1. Furosemide
  2. Acetazolamide
  3. Mannitol

K+ SPARING: (SAT)

  1. Spironolactone
  2. Amiloride
  3. Triamterene
20
Q

Where is most calcium stored?
How much is in ICF? ECF?

How does acidosis affect free ionized Calcium concentration?
Alkalosis?

A

Calcium stored in bone –> 99%
ICF –> 1%
ECF –> 0.1%

Acidosis –> increased ionized Calcium = HYPERCALCEMIA

Alkalosis –> decreased ionized Calcium –> Hypocalcemia

ex: hyperventilation: results in respiratory alkalosis & decreases free Ca2+, thus the membrane is more excitable and people become irritated –> Hypocalcemia!!

21
Q

What is the affect of PTH on calcium? How does this change Calcium excreted/reabsorbed in the kidneys? In bone?

A

PTH –> protects against low Ca2+
- senses low Calcium and increases reabsorption of Calcium by kidneys and increases bone resorption (breakdown) and increases CALCITROL which INCREASE FREE CALCIUM

22
Q

How do the following affect Calcium:

  1. PTH
  2. Calcitrol
  3. Calcitonin
A
  1. PTH –> prevents low Calcium by increasing reabsorption in kidney and resorption in bone marrow
  2. Calcitrol –> prevents low Calcium by increasing calcium resorption from bone & decreasing calcium excretion
  3. Calcitonin –> prevents HIGH CALCIUM: increases calcium deposition in bone & increases calcium excretion
23
Q

What is the affect of Calcitrol on calcium? How does this change Calcium excreted/reabsorbed in the kidneys? In bone?

A
  1. Calcitrol protects against low Ca2+
  • senses decreased calcium or [HPO4]2- or [H2PO4]-
  • Proximal tubule produces CALCITROL
  • caclium resorption from bone and decreased calcium excretion
  • increased [Ca2+]
24
Q

Where is Calcitrol released from in the nephron?

A

Proximal Tubule!

25
Q

What is the affect of CALCITONIN on calcium? How does this change Calcium excreted/reabsorbed in the kidneys? In bone?

A

Calcitonin (felon :)) protects against HIGH CALCIUM

  1. senses increased calcium
  2. increased Calcitonin
  3. Increased [Ca2+] deposition in bone
  4. Decreased [Ca2+] and increased Calcium excretion

= decreased [Ca2+]

26
Q

How much of filtered calcium is reabsorbed in the nephron? What mechanisms facilitate the reabsorption of Calcium?

A

99%

  • active & passive transport via transcellular and paracellular pathways
  • Ca-ATPase and 3Na/Ca Antiporter
27
Q

How is Calcium EXCRETION regulated?

A

Hromonally via PTH, Calcitrol, and Calcitonin

28
Q

How does PTH affect plasma [phosphate] and excretion?

A

Increases plasma phosphate and excretion

- increases plasma calcium concentration via bone resorption

29
Q

How does Calcitonin affect plasma [phosphate] and excretion?

A

decreases plasma [phosphate] and decreases excretion

- also DECREASES plasma Calcium (via deposition)

30
Q

How does Calcitrol affect plasma [phosphate] and excretion?

A

increases plasma phosphate and DECREASES excretion

-also increases plasma Calcium via bone resorption

31
Q

How does the kidney protect plasma [phosphate] from going too high aka the “spill-over” affect?

A

By keeping plasma [phosphate] very close to the RPT

  • protects the plasma from high phosphate levels by regulating its excretion/reabsorption
32
Q

How does alpha 1 receptor stimulation of epinephrine affect K+? B2?

A

alpha 1 = K+ OUT of cell –> action potential generated (vasoconstriction)

B2 = K+ INTO the cell –> vasodilation

33
Q

State how the following affect Calcium & phosphate Excretion & plasma concentrations:

  1. PTH
  2. Calcitriol
  3. Calcitonin
A
  1. PTH:
    a) increased [Ca2+] and [phosphate]
    b) decreased Calcium excretion, increased phosphate excretion
  2. Calcitriol:
    a) increased [Ca2+] and [phosphate]
    b) decreased Calcium excretion, DECREASED phosphate excretion
  3. Calcitonin:
    a) Decreased [Ca2+] and [phosphate]
    b) increased Calcium excretion, and INCREASED phosphate excretion

FHB - Pulmonary & Renal - Exam 2 (21 decks)

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