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
K+ handled in nephron through
Filtration Reabsorption Secretion
26
in FILTRATION of K+
It is not bound to plasma so freely filters
27
In REABSORPTION of K+ in PCT and TAL
PCT absorbs 67% of filtered K+ | TAL absorbs 20%
28
Which part of nephron is responsible for adjustments in K+ when dietary K+ changes
Distal tubules and collecting ducts
29
In a low K+ diet, which cells involved
K+ is reabsorbed (because there is not many so we want to reabsorb it all) by A-INTERCALATED CELLS
30
Urinary K+ excretion in a low K+ diet
<1%
31
On a high K+ diet, which cells are involved
K+ secreted by PRINCIPAL CELLS (K+ passes to renal tube from capillaries)
32
Urinary K+ excretion at high protein diets
As high as 110%
33
Reabsorption in proximal convoluted tubule and thick ascending limb is
CONSTANT under most conditions
34
Excretion in late distal tubule and collecting ducts is
VARIABLE because they perform fine-tuning of K+ excretion to maintain K+ balance
35
Type A cells function
During HYPOKALEMIA/ACIDOSIS K+ reabsorption by a-intercalated cells H+ secretion
36
Type B cells function
During HYPERKALEMIA/ALKALOSIS H+ reabsorption K+ secreted by B-intercalated cells
37
H+ and K+ secretion/reabsorption
Is the opposite | If H+ is reabsorbed (HYPERKALEMIA/ALKALOSIS) then K+ is secreted
38
Magnitude of K+ secretion determined by
Size of electrochemical gradient for K+
39
Aldosterone, acid-base disturbances, dietary K+ all increase
Impact secretion of K+
40
Dietary K+ process
``` Increase in intracellular K+ Increase in K+ in intercalated cells HYPERKALEMIA (Type B intercalated cells) K+ increased SECRETION Increased K+ in urine ```
41
Aldosterone effect on Na+
Increases Na+ reabsorption by inducing Na+/K+ATPase | Increased K+ secretion
42
What channels does an increase K+ impact (HYPERKALEMIA)
Na+/K+ATPase | ROMK channels
43
High Na+ diet impact on K+
Increase in Na+ to principal cells Increase Na+ extruded from cell through Na+/K+ATPase pumps Increase K+ into cell Increase K+ excretion
44
What are diuretics
Pills that reduce Na+ and H2O | Block Na+ reabsorption
45
Impact of diuretics in K+
Diuretics block Na+ reabsorption | Increase K+ excretion
46
What do diuretics block
Aldosterone function (which is to increase Na+/K+ATPase)
47
Increase flow rate impact on K+ secretion
Increase flow rate increases K+ secretion | More flow = more diluted K+
48
During acidosis and alkalosis, impact on K+ flow
Acidosis (high H+ in blood) = K+ out of cell | Alkalosis (low H+ in blood) = K+ into cell
49
During acidosis, which pump is inhibited
Na+/K+ATPase so K+ leaves the cell to maintain neutrality = hypokalemia
50
During alkalosis, movement of H+ and K+
H+ leaves the cell for buffering | K+ enters to maintain electroneutrality which causes hypokalemia
51
Main external buffer systems
Bicarbonate and phosphate
52
In volume depletion, aldosterone stimulates
Na+ retention without K+ secretion
53
In hyperkalemia there is stimulation of
K+ secretion w/ salt retention
54
During hypovolemia, mechanism of AngiotensinII
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
During hyperkalemia, aldosterone and angiotensin II effect
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
Where is the Na+/Cl- cotransporter
In early distal convoluted tubules