K+ metabolism Flashcards

1
Q

Normal American diet contain approximately ___ meq of K

A

100 meq

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2
Q

What is the intracell conc on K+?

A

120-140 meg

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3
Q

What is the extracell conc of K+?

A

4-5 meq

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4
Q

Where is the majority of K+ stored?

A

muscle

*other significant storage include liver, RBC, and bone

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5
Q

If the kidney is functioning normally, ____% of dietary K+ is excreted through the kidney

A

almost 100

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6
Q

What is internal K+ balance?

A

regulation of the distribution of K+ between the ICF and ECF

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7
Q

What is K+ external balance?

A

regulation of TBk+ thru alterations in K+ intake and excretion (GI, renal)

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8
Q

Where does most of the K+ reabs occur?

A

PT and TALH

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9
Q

Where is the only place K+ is secreted?

A

principal cells in cortical and outer medullary CD

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10
Q

How much K+ is reabs in the PT?

A

65%

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11
Q

How much K+ is reabs in the TALH?

A

35%

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12
Q

Describe the movement of K+ in cells at TALH

A

Basolateral:
-NaK-ATPase antiport brings K+ into the cell

Apical:

  • NaKCl co transporter brings K+ into cell
  • K+ channel brings K+ out of cell and into lumen (moves here bc the Na reabsorption creates a - charge in lume)

-paracellular diffusion from lumen to blood thru tight junction

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13
Q

What happens to the K+ that flows into the lumen thru the apical K+ channel?

A

Not excreted!

  • “re-used” for NaKCl co-transporter
  • creates a + charge in lumen to repel other cations (Na, K, Ca, Mg) to be transported/diffuse paracellularly
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14
Q

Is K+ normally excreted?

A

no, its almost 100% reabs

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15
Q

WHat effect does also have on the principal cells in the CD?

A

goes into the nucleus to bind a nuclear receptor to inc the expression of

  1. Na-K pump
  2. Na epithelial channel (apical side)
  3. K+ channel (apical side)
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16
Q

What are the factors that effect K+ secretion?

A
  1. conc gradient (high serum K+ –> inc secretion)
  2. electrical gradient (Na needs to have been reabs in PT to create a - charge in lumen)
  3. K+ permeability (# open K+ channels on luminal side <-aldo)
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17
Q

graph slide

A

9

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18
Q

What are causes of decreased renal potassium secretion (4)?

A
  1. renal failure
  2. DT dysfunction (part of the kidney that secreted K+)
  3. decreased distal tubular flow = decrease in distal delivery of Na
  4. hypoaldosteronism or inhib of aldo
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19
Q

What are causes of hyperkalemia?

A

same as those that decrease K+ secretion

  1. renal failure
  2. DT dysfunction (part of the kidney that secreted K+)
  3. decreased distal tubular flow = decrease in distal delivery of Na
  4. hypoaldosteronism or inhib of aldo
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20
Q

Slides

A

11

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21
Q

slide

A

12

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22
Q

What can cause increased reanl potassium secretion?

A
  1. diurretics (loops and thiazide)
  2. prolonged vomiting
  3. nasogastric suction
  4. Bartter’s syndrome
  5. Gitelman’s syndrome
  6. hyperadosteronism

*inc secretion caused hypokalemia

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23
Q

How do diurectic, vomiting, and Bartter’s and Gitelman’s cause hypokalemia?

A

increase distal Na deliver –> increase K secretion

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24
Q

How is internal K balance maintained?

A

adjusting K transport across the cell membrane

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25
Q

The concentration gradient of K (ICF > ECF) is responsible for passive transport of ____ through _____.

A

K+ thru K+ channels

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26
Q

T or F: the concentration gradient of K between intracellular and extracellular fluid is maintained by transporting K from extracellular fluid to cells against the concentration gradient.

A

true

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27
Q

What is the main pathway to transport if K into cells?

A

NaK-ATPase

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28
Q

The NaK ATPase pump transports ___ Na out of the cells and ___ k into the cells

A

3 Na out and 2 K in

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29
Q

T or F: all the factors that affect the internal K balance works through the NaK ATPase pump

A

T

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30
Q

What are 7 factors that affect the internal balance of K+?

A
plasma K conc
insulin 
Epi
Acid base disturbance
plasma tonicity 
cell lysis
cell proliferation
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31
Q

How does an inc in plasma K+ affect the internal balance of K+?

A

inc in plasma [K+] decreases K+ movement outside of the cell

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32
Q

How does insulin affect the internal balance of K+?

A

insulin moves K+ inside cells by

  1. stimulates NaH exchanger to move Na inside the cell. T
  2. this activates NaK ATPase pump
  3. K+ is moved inside cells
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33
Q

How does epinephrine affect the internal balance of K+?

A

Stimulates Beta2 receptor which activates the NaK ATPase –> K+ goes into cells

34
Q

WHat effect does activation of the alpha 2 receptor have on K+ internal balance?

A

activation of alpha 2 inhibits the NaK ATPase and will inc plasma K+

35
Q

How can diabetes effect the K+ plasma levels?

A

they have defcicint insulin = dec activity of NaK ATPase = more K+ in ECF

*the K+ channel will not not be affected by hormones and will continue to move K+ from the ICF–> ECF

36
Q

What affect does albuterol have on a plasma K+ levels?

A

it binds Beta2 receptor to stimulate the NaK-ATPase (moves K+ from ECF to ICF)
*Tx for hyperkalemia

37
Q

How will an acid base disturbance affect internal balance of K+?

A

dec in pH –> hyperkalemia

inc pJ –> hypokalemia

38
Q

T or F: respritory acid-base distrubances have a greater effect than metabolic acid-base disturbances

A

F: metabolic disturbances have a greater effect and respiratory

39
Q

T or F: Metabolic acidosis due to organic acids (ketoacidosis, lactic acidosis) have smaller effects than do acidosis due to mineral acids

A

T

40
Q

How does tonicity affect the internal balance of K+?

A

hypertonicity (i.e. hypernatremia or hyperglycemia) or hyperosmolar in the ECF will cause water to flow from ICF to ECF. The water that flows from the ICF will drag K+ with it as it moves (solvent drag)

Also, as water moves out it of the ICF, the intracellular concentration increases –> increases the conc gradient –> more K+ moves into ECF thru the K+ cannel

–> hyperkalemia

41
Q

What effect does a state of diabetic ketoacidosis have on the K+ internal balance?

A

in diabetic ketoacidosis, there is a hyperosmolar/hypertonic state in the ECF (hyperglycemia) that cuases water to flow into ECF, dragging K+ with it and inc intracell cocn of K+ –> K+ moves with the conc/into ECF thru K+ channels

Acidosis also contributes to hyperkalemia

42
Q

How does cell lysis affect the internal balance of K+?

A

when a cell lysis it releases the K+ that was stored in the cell into the extracell space

*ex: rhabdomyolysis, RBC injury/hemolysis

43
Q

How does cell proliferation affect the internal balance of K+?

A

K+ is rapidly taken up by proliferating cells, causing extracell K+ to decrese = hypokalemia

44
Q

Leukemia will cause a (hyper- or hypo-) kalemic state.

A

hypo (cell proliferation rapidly takes up extracell K+)

45
Q

Hyperkalemia is considered to be > ____ meq/L of potassium.

A

> 5.5 meq/L

46
Q

What are 3 general cuases of hyperkalemia? (think like Dr. Nace)

A
  1. too much intake
  2. decrease excretion
  3. internal redistribution
47
Q

Hyperkalemia can be caused by decreased renal excretion, what specifically can cause that?

A

acute or chronic renal failure
dec distal tubular flow
distal tubular dysfunction (where is it secreted
hypo-aldosteronism

48
Q

What can cause an internal redistribution of K+ leading to hyperkalemia?

A
insulin deficiency
Beta2 adrenergenic blockade
hypertonicity
acidemia
cell lysis
49
Q

Describe the EKG manifestations of hyperkalemia.

A

plasma K+ mEq/L –> EKH changes
4 –> normal
6 –> peaked T waves
8 –> wide QRS complex, shortened QT interval, prolonged PR interval
10 –> further widening of QRS complex, absent P wave
12 –> sine wave morphology (ventricular tachycardia)

50
Q

What are the sigs and symptoms of hyperkalemia?

A

Cardiac:

  • EKG changes
  • cardiac conduction defects
  • arrhythmias (bradyarrythmia)

Neuromuscular:

  • asceending weakness
  • ileus
51
Q

What are the treatment options for hyperkalemia?

A
  1. Sblz cardiac muscle cells
  2. lower serum K+ by moving K+ inside cells
    • insulin, Beta agonists, Bicarbonate
  3. lower serum K+ by moving K+ outside the body
    • diuretics, cation exchange resins, dialysis
52
Q

Where does insulin act to treat hyperkalemia?

A

inc activity of Na:H ion exchanger

53
Q

Where does bivarbonate act to treat hyperkalemia?

A

inc activity of Na:H exhanger

54
Q

Will insulin cause acidosis?

A

no, but it needs to be given with glc to prevent hypoglycemia

*apparently, it doesn’t inc extracell [H+] enough to cause acidosis

55
Q

What treatment option for hyperkalemia is the quickest?

A

Calcium

56
Q

How does calcium admin treat hyperkalemia?

A

antagonizes membrane depolarization from in extracell K+

57
Q

What is the root cause of most of the signs and symptoms assc with hyperkalemia?

A

from the depolarization of resting cell membrane potential in myocytes and neurons

*Prolonged depolarization decreases membrane Na+ permeability through the inactivation of voltage-sensitive Na+ channels producing a reduction in membrane excitability

58
Q

Hypokalemia is considered to be < ____ meq/L of potassium.

A

< 2.5 mEq/L

59
Q

What are the 3 general causes of hypokalemia? (think like Dr. Nace)

A

decreased intake
increased renal excretion
internal redistribution

60
Q

How is K+ lost externally?

A

GI, skin, renal

61
Q

What causes K+ to be redistributed internally leading to hyokalemia?

A

insulin excess
catecholamine excess
alkalemia
cell proliferation

62
Q

What can be a cause of hypokalemia with normal BP and metabolic alkalosis?

A
loop and thiazide diuretics 
prolonged vomiting
nasogastric suction 
Bartter's syndrome
Gitleman's syndrome
63
Q

What can be a cause of hypokalemia with normal BP and metabolic acidosis?

A
RTA
uretral diversion (uretero-ileostomy, utereo-sigmoidostomy)
64
Q

How does RTA II cause hypokalemia?

A

prevents reabs if K+ in PT

65
Q

How does Girleman’s cause hypokalemia?

A

blocks NaCl transporter

66
Q

How can thiazides cause hypokalemia?

A

blocks NaCl transporter

67
Q

How does RTA I cause hypokalemia?

A

defect in CD that increases K+ excretion in the urine

68
Q

How cam furosemides cause hypokalemia?

A

blocks NaKCl channel and delivers more K to CD

69
Q

How does Bartter’s cause hypokalemia?

A

blocks NaKCl channel and delivers more K to CD

70
Q

What are hypertensive disorders assc with hypokalemia?

A

hyperreninemia
Conn’s syndrome (primary hyperaldosteronism)
Cushing’s syndrome (glucocorticoid excess)
congenital adrenal hyperplasia

71
Q

What can cause hyperrninemia leading to hypokalemia?

A

renal artery senosis (inc RBF and signals for renin production)

renin-secreting tumor

72
Q

What can cause conn’s syndrome leading to hypokalemia?

A

adrenal hyperplasia and adrenal tumors

*inc aldo which inc NaK ATPase activity and the number of luminal K channels

73
Q

What can cause cushing’s syndrome leading to hypokalemia?

A

exogenous, pituitary, or adrenal production of excess glucocorticoids

*works just like also to nc NaK ATPase activity and the number of luminal K channels

74
Q

How does congenical adrenal hyperplasia lead to hypokalemia?

A

there are enzymatic defects in cortisol biosynthesis –> excess aldo precursor –> inc aldo –> inc NaK ATPase activity and the number of luminal K channels

75
Q

What are the clinical manifestations of acute hypokalemia?

A

Cardiac:

  • EKG changes
  • arrhythmias-tachyarrythmias

Smooth muscle:

  • hypertension
  • ileus

Skeletal musle:

  • weakness
  • rhabdomyolysis

Renal:
-nephrogenic diabetes insidius

76
Q

Describe the EKG manifestations of hypokalemia.

A

normal –>
Flat T wave –>
prominant U wave –>
Depressed ST segment

77
Q

What are the clinical manifestations of chronic hypokalemia?

A

asymptomatic

78
Q

What is the treatment for hypokalemia?

A

K+ replacement (give large amounts slowly)

  • given usually as KCL, KPO4
  • oral or IV

K+ sparing diuretics

  • eNaC inhib (amiloride, triamterene)
  • mineralcorticoid antagonists (spironalactone, eplerenone)
79
Q

What are the 2 most important determinants of K+ secretion?

A

aldo levels

distal Na delivery

80
Q

T or F: both high and low serum K+ levels can result in serious cardiac rhythm abnormalities

A

T