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Histology > Exam 3 Lecture - Regulation of Potassium > Flashcards

Exam 3 Lecture - Regulation of Potassium Flashcards

1
Q

What is the main intracellular cation?

A

potassium

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2
Q

What is K important for inside of cells?

A

an important osmole, maintaining cell volume

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3
Q

Why is K important extracellularly?

A

to avoid the affects of hypokalemia and hyperkalemia

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4
Q

What is hypokalemia?

A

low levels of extracellular potassium

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5
Q

What is hyperkalemia?

A

high levels or extracellular potassium

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6
Q

Does the kidney regulate intracellular or extracellular potassium?

A

extracellular potassium

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7
Q

How does hypokalemia affect the generation of action potentials?

A

it makes generating them harder because it makes the resting membrane potential lower

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8
Q

How does hyperkalemia affect the generation of action potentials?

A

it makes generating action potentials easier, but Na levels inside of the cell are unable to reset, so the cell becomes less excitable

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9
Q

What are symptoms associated with hypokalemia?

A

muscle weakness, respiratory problems, cardiac arrhythmia, renal dysfuntion

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10
Q

What are symptoms associated with hyperkalemia?

A

muscle weakness and cardiac dysfunction

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11
Q

Is hypokalemia or hyperkalemia worse?

A

hyperkalemia

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12
Q

If enough K is not excreted, what will happen to the animal?

A

it will become hyperkalemic

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13
Q

If too much K is excreted, what will happen to the animal?

A

it will become hypokalemic

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14
Q

Where does the most K excretion occur?

A

in the kidney

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15
Q

What is the kidney’s short term response to an altered K concentration outside of the cell?

A

translocation: sends K out to the ECF it is too low, sends K into the cell if ECF is too high

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16
Q

What is translocation affected by?

A

insulin, catecholamines, acidosis/alkalosis

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17
Q

What is insulin given to correct?

A

hyperkalemia

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18
Q

How do catecholamines work?

A

they can move K in and out depending on whether they activate alpha or beta receptors

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19
Q

What is bicarb administered to correct?

A

hyperkalemia

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20
Q

How does insulin correct hyperkalemia?

A

it promotes movement of K into cells by stimulating NaKATPase

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21
Q

What receptors are associated with catecholamines?

A

alpha and beta

22
Q

Do alpha receptors promote the movement of K into the cell or out of it?

A

out of it

23
Q

Do beta receptors promote the movement of K into the cell or out of it?

A

into it by stimulating NaKATPase

24
Q

What does acidosis promote in regards to potassium movement?

A

hyperkalemia - High H+ promotes movement of K out of the cells in order to maintain electroneutrality - but into the ECF

25
Q

What does alkalosis promote in regards to potassium movement?

A

hypokalemia - Low H+ moves K into cells - but into the ECF

26
Q

Under normal conditions what is the primary goal of the kidney in regards to K?

A

to retain it

27
Q

What function must the kideny have in order to maintain homeostasis?

A

to secrete K

28
Q

True or False: The proximal tubule can only secrete K.

A

False: the proximal tubule can only reabsorb K, it cannot secrete it

29
Q

How is K reabsorbed in the proximal tubule?

A

paracellularly and transcellularly

30
Q

Where can K be reabsorbed paracellularly in the proximal tubule?

A

only in the late proximal tubule

31
Q

How is K reabsorbed in the proximal tubule transcellularly?

A

by the K Cl symporter in the basolateral membrane ‘ there are probably K channels in the luminal membrane too’

32
Q

True or False: The distal tubule can only absorb K, and cannot secrete it

A

True

33
Q

How is K reabsorbed in the distal tubule?

A

paracellularly and transcellularly

34
Q

How is K reabsorbed transcellularly in the distal tubule?

A

via the NKCC1 transporter at the luminal membrane and K channels in the basolateral membrane

35
Q

Is K reabsorbed or secreted in the collecting ducts?

A

both

36
Q

Where is K secreted in the collecting ducts?

A

in the principle cells

37
Q

How is K secreted in the collecting ducts?

A
  1. NaKATPase keeps intracellular K concentration high
  2. Na enters viathe amiloride-sensitive channels making the lumen negative
  3. K wants to move out of the cell and does so on the luminal side because it is more permeable to K (some does leave through the basolateral side
38
Q

What part of the collecting ducts reabsorb K?

A

the alpha intercalated cells

39
Q

How is K reabsorbed in the alpha intercalated cells?

A
  1. H leaves the cell via HATPase,
  2. H K ATPase brings K in at the luminal membrane
  3. K then leaves at the basolateral membrane into the extracellular fluid
40
Q

What determines renal K excretion?

A

plasma K concentration, tubular flow rate, lumen electronegativity

41
Q

What does increased plasma concentration of K lead to?

A

the translocation into the ICF increasing the K gradient in renal cells and pushing K into the lumen
also stimulates aldosterone

42
Q

How does aldosterone affect K excretion?

A

it stimulates Na reabsorption which means K is being pushed out of the cells (Na channels and K channels are increased)

43
Q

What does hyperaldosteronism lead to?

A

hypokalemia

44
Q

What does hypoaldosteronism lead to?

A

hyperkalemia

45
Q

How does decreased tubular flow rate affect K secretion?

A

it decreases it

46
Q

How does increased tubular flow rate affect K secretion?

A

it increases it

47
Q

How does increased lumen electronegativity affect K secretion?

A

it increases it

48
Q

How does decreased lumen electronegativity affect K secretion?

A

it decreases it

49
Q

How does Na intake affect renal handling of K?

A

increased dietary intake of Na leads to increase of tubular concentration therefore more Na reabsorption and more K secretion

50
Q

How do loop, thiazide, and osmotic diuretics affect renal handling of K?

A

increase the flow rate and Na concentration in CD which increases K secretion and can cause hypokalemia

51
Q

How do amiloride-like diuretics affect renal handling of K?

A

inhibit Na uptake in CD so inhibit K secretion; known as K sparing diuretics

Histology (36 decks)

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