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RENAL > V: Potassium Balance > Flashcards

V: Potassium Balance Flashcards

1
Q

Postassium balance has to be kept

A

CONSTANT

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2
Q

% K+ in ICF

A

98%

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3
Q

% K+ in ECF

A

2%

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4
Q

Hyperkalemia values

A

K+ > 5meq/L

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5
Q

Hypokalemia values

A

K+ < 3.5meq/L

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6
Q

Consequences of hyperkalemia and hypokalemia

A

Weakness
Paralytic ileus
Cardiac arrythmia

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7
Q

Internal K+ balance depends on

A

Hormones
Drugs
Pathological state

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8
Q

External K+ balance is

A

Urinary K+ excretion = Dietary K+

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9
Q

What 3 hormones released after K+ ingestion

A

Insulin
Catecholamines
Aldosterone

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10
Q

Insulin effect

A

Stimulates K+ uptake through increase in Na+/KATPase

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11
Q

Sympathetic nervous system effect

A

Through B2 receptors, increase in Na+/K+ATPase

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12
Q

Increase in Na+/K+ATPase promote

A

K+ into the cell which can result in HYPOKALEMIA

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13
Q

On the other hand, a receptors cause

A

K+ to move out of cell and cause Hyperkalemia

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14
Q

Aldosterone effect

A

Increases Na+/K+ATPase

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15
Q

Not pathological situations where an alteration in extracellular K+ may occur due to disturbance in internal K+ balance

A

Exercise as K+ moves out of cells
Acid-base abnormalities, H+/K+ exchange. As H+ leaves the cell, K+ has to accompany it, leading to disturbance in external balance

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16
Q 
During alkalemia
pH
[H+] blood
H+ movement
K+ movement
A

pH>7.45
[H+] decreased
H+ moves out of cells
K+ enters cells

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17
Q 
During acidemia 
pH
[H+] blood
H+ movement
K+ movement
A

pH<7.35
[H+] increased
H+ into cells
K+ leaves cells

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18
Q

K+ movement compared to H+

A

K+ follows the opposite movement from H+

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19
Q

Shift of K+ during hyperosmolarity

A

Hyperosmolarity is when there a decrease in H2O

H2O leaves the cell and drags K+ along with it

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20
Q

Cell lysis effect on K+

A

Releases K+ causing hyperkalemia

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21
Q

Agonist vs antagonist

A

Agonist is a drug that binds to its receptor to produce a similar response
Antagonist does not allow receptor to follow response

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22
Q

K+ shifts into cell: HYPOKALEMIA

A 
Insulin 
B-2 Adrenergic agonist
A-adrenergic antagonist 
Alkalosis 
Hyposmolarity (too much H2O)
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23
Q

K+ shifts out of cell: HYPERKALEMIA

A 
Insulin deficit
B-2 Adrenergic antagonist
Acidosis
Hyperosmolarity (decrease H2O)
Cell lysis 
Exercise
24
Q

Why are external balance mechanisms flexible

A

Because K+ varies a lot

25
Q

K+ handled in nephron through

A

Filtration
Reabsorption
Secretion

26
Q

in FILTRATION of K+

A

It is not bound to plasma so freely filters

27
Q

In REABSORPTION of K+ in PCT and TAL

A

PCT absorbs 67% of filtered K+

TAL absorbs 20%

28
Q

Which part of nephron is responsible for adjustments in K+ when dietary K+ changes

A

Distal tubules and collecting ducts

29
Q

In a low K+ diet, which cells involved

A

K+ is reabsorbed (because there is not many so we want to reabsorb it all) by A-INTERCALATED CELLS

30
Q

Urinary K+ excretion in a low K+ diet

A

<1%

31
Q

On a high K+ diet, which cells are involved

A

K+ secreted by PRINCIPAL CELLS (K+ passes to renal tube from capillaries)

32
Q

Urinary K+ excretion at high protein diets

A

As high as 110%

33
Q

Reabsorption in proximal convoluted tubule and thick ascending limb is

A

CONSTANT under most conditions

34
Q

Excretion in late distal tubule and collecting ducts is

A

VARIABLE because they perform fine-tuning of K+ excretion to maintain K+ balance

35
Q

Type A cells function

A

During HYPOKALEMIA/ACIDOSIS
K+ reabsorption by a-intercalated cells
H+ secretion

36
Q

Type B cells function

A

During HYPERKALEMIA/ALKALOSIS
H+ reabsorption
K+ secreted by B-intercalated cells

37
Q

H+ and K+ secretion/reabsorption

A

Is the opposite

If H+ is reabsorbed (HYPERKALEMIA/ALKALOSIS) then K+ is secreted

38
Q

Magnitude of K+ secretion determined by

A

Size of electrochemical gradient for K+

39
Q

Aldosterone, acid-base disturbances, dietary K+ all increase

A

Impact secretion of K+

40
Q

Dietary K+ process

A 
Increase in intracellular K+
Increase in K+ in intercalated cells 
HYPERKALEMIA (Type B intercalated cells)
K+ increased SECRETION 
Increased K+ in urine
41
Q

Aldosterone effect on Na+

A

Increases Na+ reabsorption by inducing Na+/K+ATPase

Increased K+ secretion

42
Q

What channels does an increase K+ impact (HYPERKALEMIA)

A

Na+/K+ATPase

ROMK channels

43
Q

High Na+ diet impact on K+

A

Increase in Na+ to principal cells
Increase Na+ extruded from cell through Na+/K+ATPase pumps
Increase K+ into cell
Increase K+ excretion

44
Q

What are diuretics

A

Pills that reduce Na+ and H2O

Block Na+ reabsorption

45
Q

Impact of diuretics in K+

A

Diuretics block Na+ reabsorption

Increase K+ excretion

46
Q

What do diuretics block

A

Aldosterone function (which is to increase Na+/K+ATPase)

47
Q

Increase flow rate impact on K+ secretion

A

Increase flow rate increases K+ secretion

More flow = more diluted K+

48
Q

During acidosis and alkalosis, impact on K+ flow

A

Acidosis (high H+ in blood) = K+ out of cell

Alkalosis (low H+ in blood) = K+ into cell

49
Q

During acidosis, which pump is inhibited

A

Na+/K+ATPase so K+ leaves the cell to maintain neutrality = hypokalemia

50
Q

During alkalosis, movement of H+ and K+

A

H+ leaves the cell for buffering

K+ enters to maintain electroneutrality which causes hypokalemia

51
Q

Main external buffer systems

A

Bicarbonate and phosphate

52
Q

In volume depletion, aldosterone stimulates

A

Na+ retention without K+ secretion

53
Q

In hyperkalemia there is stimulation of

A

K+ secretion w/ salt retention

54
Q

During hypovolemia, mechanism of AngiotensinII

A

In hypovolemia we want to increase Na+ reabsorption (bc H2O follows it) to increase extracellular volume
Angiotensin II –> Aldosterone
Aldosterone will increase ENaC, so more Na+ rebasorbed
Angiotensin II will promote Na+/Cl- cotransport
Angiotensin II will inhibit ROMK, K+ secretion

55
Q

During hyperkalemia, aldosterone and angiotensin II effect

A

We want to decrease K+ in cell, so K+ excretion
Aldosterone will promote ENaC and ROMK, Na+ and K+ secretion
Angiotensin II will block Na+/Cl- cotransport

56
Q

Where is the Na+/Cl- cotransporter

A

In early distal convoluted tubules

RENAL (9 decks)

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