Potassium Metabolism

Front 1

How is K distributed in the human body? Where is most of it? What is intracellular K concentration? What is extracellular? Where is the majority excreted?

Back 1

Front 2

K concentration in the body is maintained how?
Internal balance of K is maintained by regulation of what?

Back 2

Front 3

Identify the places where urinary potassium is excreted in the nephron. Where is K reabsorbed?

Back 3

Front 4

How does K+ enter and exit in cells of the thick ascending loop of Henle?

Back 4

Front 5

How does potassium enter the lumen in principal cells in the CCT and outer medullary CT?
What causes this?

Back 5

Front 6

What are the factors that affect K secretion in the CT? What is the final step in K secretion affected by?

Back 6

1. Concentration gradient of K across cell membrane (depends upon serum K concentration)
2. Electrical gradient across cell membrane (depends upon reabsorption of Na through Na channels in luminal membrane --> depends upon Na tubular lumen concentration --> distal delivery of Na.
3. K-permeability of the luminal membrane

Front 7

What if Na is not reabsorbed in the earlier part of the tubules (PCT or loop of Henle)?

What if the opposite occurs?

Back 7

More Na will be delivered tot he collecting tubule --> more Na reabsorption by ENa channel and K loss.

Not a large distal delivery --> will impair K secretion in collecting tubule

Front 8

What does K permeability of luminal membrane depend upon? What is this affected by?

Back 8

Number of open K channels on luminal membrane

Aldosterone combines with receptor in the cells and increases the number of open luminal Na channels --> increase in NaK ATPase activity and open up K channel.

Front 9

What will the increase in aldosterone cause?
What will inhibition of aldosterone cause?

Back 9

Hypokalemia
Hyperkalemia?

Front 10

How does distal tubular flow rate affect distal potassium secretion?

Back 10

Front 11

What factors will decrease renal potassium secretion?

What will all of these factors also cause?

Back 11

Renal failure, distal tubular dysfunction, decreased distal tubular flow, hypoaldosteronism (will cause hyperkalemia).

Increased serum K levels (hyperkalemia)

Front 12

What can cause increased renal potassium secretion (4 categories)?

Back 12

Diuretics (loop and thiazide), prolonged vomiting/nasogastric suction, Bartter's Syndrome/Gitelman's syndrome, hyperaldosteronism

Front 13

How is internal potassium balance maintained?

Back 13

By adjusting the K transport across the cell membrane (Na+ K+ ATPase is energy dependent)

Front 14

How is K transported into cells?

Back 14

NaKATPase (3Na+ in for every 2K+ out)
Requires energy
Main pathway to transport K inside cells
ALL FACTORS THAT AFFECT K INTERNAL BALANCE WORK THROUGH THIS PUMP.

Front 15

What three factors favor K movement across the cell membrane?
What can directly affect the K diffusion out of the cells?

Back 15

1. Plasma K concentration
2. Insulin
3. Epinephrine

PLASMA K CONCENTRATION

Front 16

Describe the effect of insulin.

Back 16

Insulin moves K inside the cells, but it does not directly work on this pump. Instead, insulin stimulate a NaH exchanger on the cell membrane that moves Na inside the in exchange for Na, this intracellular Na than activate the NaKATPase pump and moves K inside the cells. Other hormone epinephrine activate the NaKATPase pump by stimulating beta receptor. If there is deficiency of insulin as it happens in diabetic patients, or if we block the beta receptor by beta blocker, the activity of NKATPase pump will be impaired, with decrease movement of K from ECF to ICF. But the K channel which is not affected by the hormones will remain open and will continue to move K ICF to ECF which will result in elevated K in ECF.

Front 17

What are some factors affecting internal balance of potassium?

Back 17

Acid-base distubance
Plasma tonicity
Cell lysis and cell proliferation

Front 18

How do acid base disturbances affect internal balance of potassium? Which have a greater effect (metabolic or respiratory)?
With regard to organic acids or mineral acids, which have a greater effect?

Back 18

Front 19

How does plasma tonicity affect internal balance of potassium?

Back 19

Front 20

Does plasma tonicity or osmolality also affect serum K? How?

What conditions will this happen in?

Back 20

Hypertonic ECF --> movement of ICF water to ECF, when water moves out of the cell, drags K along with it. (SOLVENT DRAG)
Water movement out of cell with ECF hypertonicity increases intracellular K, which increases gradient between ICF and ECF --> more K diffusion out through K channel --> hyperkalemia

Diabetic ketoacidosis or diabetic hyperosmolar state --> ECF tonicity due to elevated glucose concentration

Front 21

How does cell lysis and cell proliferation affect internal balance of potassium?

Back 21

Front 22

What are some causes of hyperkalemia?

Back 22

Front 23

What are some causes of excessive potassium intake?

Back 23

Oral or parenteral intake

Front 24

What are some causes of decreased renal excretion?

Back 24

Front 25

What are some causes of internal redistribution?

Back 25

Front 26

What are some EKG manifestations of hyperkalemia?
Put them in order serum K?

Back 26

Front 27

What are some signs and symptoms of hyperkalemia? Think cardio and neuro.

Back 27

Front 28

What do clinical manifestations of hyperkalemia primarily result from?

What does prolonged depolarization cause?

Back 28

Depolarization of resting cell membrane potential in myocyes and neurons.

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

Front 29

What are the two main big things to do to treat hyperkalemia?

Back 29

Stabilize cardiac muscle cells
Lower serum K+

Front 30

What are two general ways to lower serum K+?

Back 30

Moving K inside the cells
Moving K outside the body

Front 31

How do you move K inside the cells?

Back 31

Insulin
B-agonists (albuterol)
Bicarbonate

Front 32

How do you move K outside the body?

Back 32

Diuretics
Resins (kayexalate)
Dialysis

Front 33

Where do insulin and albuterol act (net effect)?

Back 33

Potentiate the activity of Na K Atpase pump and move K inside cells

Front 34

Where does insulin also act? Where does albuterol act? (both initially)

Back 34

Insulin = Na+ H ion exchanger
Albuterol = B2 receptor

Front 35

Know this table?

Back 35

Front 36

What are some causes of hypokalemia?

Back 36

Front 37

What are causes of external K losses?

Back 37

Front 38

What are some causes of internal redistribution?

Back 38

Front 39

What are the two different types of renal losses that result in hypokalemia?

Back 39

Front 40

What are the two types of normotensive disorders?

Back 40

With metabolic alkalosis
With metabolic acidosis

Front 41

What are some causes of hypokalemia normotensive with metabolic alkalosis?

Back 41

Diuretics (loop, thiazide)
Prolonged vomiting, nasogastric suction
Bartter's syndrome, Gitelman's syndrome

Front 42

What are some causes of hypokalemia normotensive disorders with metabolic ACIDOSIS?

Back 42

Front 43

Where does RTAII, furosemide, Bartter's, Gitelman, Thiazides, and RTA I affect the nephron leading to hypokalemia?

Back 43

Front 44

What are some causes of hyperreninemia?
What are some causes of primary hyperaldosteronism?

How do these cause hypokalemia?

Back 44

Diuretics and these 2 syndromes cause hypokalemia by increasing distal Na delivery.

Front 45

What other two cause hypokalemia in hypertensive disorders?

Back 45

Again, by increasing distal Na delivery

Front 46

What are the major clinical manifestations of hypokalemia (general locations)? Is this in acute or chronic situations?

Back 46

1.) Cardiac
2.) Smooth muscle
3.) Skeletal muscle
4.) Renal

Acute --> chronic is asymptomatic

Front 47

What are the cardiac manifestations?

Back 47

EKG changes
Arrhythmias--Tachyarrhythmias

Front 48

What are the smooth muscle manifestations?

Back 48

Hypertension
Ileus

Front 49

What are the skeletal muscle manifestations?

Back 49

Weakness
Rhabdomyolysis

Front 50

What are the renal manifestation?

Back 50

Nephrogenic diabetes insipidus

Front 51

What are the EKG manifestations of hypokalemia? Put in order of decreasing K.

Back 51

Front 52

What is the treatment of hypokalemia?
What change indicates a deficiency of 200-400 mEq of potassium?
What is the used for treatment? Oral and intravenous

Back 52

Front 53

What diuretics are used to treat hypokalemia?

Back 53

Potassium sparing diuretics = usually in chronic, both types work on collecting tubule

ENaC sodium channel inhibitors = amiloride, triamterene
Mineralocorticoid antagonists = spironolactone, eplerenone

Front 54

How do the aldosterone receptor agonists act?
How do the ENa channel inhibitors act?

Back 54

1. Aldosterone receptor antagonists: Which act by preventing the binding of aldosterone with the aldosterone receptors.
2. ENa channel inhibitors: These act inhibiting the ENa channel Inhibiting this channel will increase the +ve charges in the lumen, which in turn will prevent K secretion.

Front 55

True or false:

1. None of the bodies potassium is intracellular.
2. All the potassium is excreted through feces.
3. Proximal tubule is the major site of potassium reabsorption.
4. Distal tubule is the major site of potassium secretion.

Back 55

1. False = almost all is INTRACELLULAR
2. False = excreted by KIDNEY
3. True
4. False = COLLECTING TUBULE is the site of potassium secretion

Front 56

What are the important determinants of potassium secretion?

Back 56

Serum aldosterone level and distal sodium delivery

Front 57

Both high and low "what" can cause serious cardiac rhythm abnormalities.

Back 57

Serum potassium levels