Lecture 49 - Potassium Balance

Question 1

value of normal extraceullar K

Answer 1

ECF K = 3.5 to 5

Question 2

Effect on the Resting membrane potential:

hyperkalemia –

hypokalemia -

Answer 2

hyperkalemia – cells closer to threshold

hypokalemia – further from threshold

Question 3

Short term homeostasis of K

Answer 3

Transcellular shifts - hiding the K in cells (myocytes, liver, RBCs)

Question 4

Long term Homeostasis of K

Answer 4

Renal excretion

Question 5

2 sites of K excretion along the tubule

Answer 5

Bowmans – K is freely filtered

Thick Ascending Loop –
Na K 2Cl (K initially absorbed, but some leaks back into the tubule)

CD: Principle Cells
(ENaC absorb Na; K excreted into tubule via ROMK)

Question 6

Overall excretion rate of K determined by what 3 factors:

Answer 6

1) Lumen Negative – which is dependent upon Na reabsorbion; makes tubule more negative, more driving force for K excretion
2) Fluid Flow Rate – High flow rate clears any existing K in the lumen; increases gradient for K to flow out of the cell
3) Aldosterone – Increases rate of ATPase, ENac and ROM K conductance

Question 7

Hypokalemia:

how do you differentiate between renal and non renal etiologies

Answer 7

Renal: UK > 20
- the kidney is not appropriately reabsorbing K that it needs

Non Renal: UK < 20
- the kidney is working fine

Question 8

Renal Etiologies of hypokalemia

Answer 8

Mineralocorticoid Excess – (eg licorice abuse, hyperaldosterone)

Diuretics –
Loop Diuretics: Block NaK 2Cl of the TAL

Thiazides: Block NaCL Co tx of early DCT

Question 9

Non renal Etiologies of Hypokalemia

Answer 9

Diarrhea

Question 10

Physiologica conesquences of Hypokalemia:

• what specific EKG changes are seen

Answer 10

§ Neuro muscular effects 
§ Renal Effects -- can lead polyuria, polydipsia 
§ Metabolic -- 
§ Vasoconstriction
§ Rhabdomyolysis 
§ Cardiac
□ EKG Changes -- 
Flattening of the T wave Development of the U wave 

Can lead to Bradyarrhythmias

Question 11

Treatment of Hypokalemia

Answer 11

Repletion –
Oral - -QUICKER

IV – limited by the amount you can give; don’t want to make the patient hyperkalemic

Question 12

causes of psuedohyperkalemia

Answer 12

Mechanical trauma

Increased WBC or PLTs – a newly dx leukemia

Question 13

Drugs which can lead to Increased K retention and lead to hyperkalemia

Answer 13

Drugs that Blunt Luminal negativity — Amiloride, bactrim

Affect Aldosterone – Blockers, K Sparing Diuretics

Question 14

3 mechanisms of hyperkalemia

which is the most common cause?

Answer 14

Redistribution – (acidemia,Hyperkalemia Periodic Paralysis after eating a high Carb meal)

Increased Input –
endogenous,
exogenous

Question 15

Increased Input of K

endogenous examples

Exogenous examples

Answer 15

Endogenous: Hemolysis, rhabdomyolosis

Exogenous: Salt substitutes; K PCNs

Question 16

Conditions of Decreased Excretion of K

Answer 16

□ Renal failure
□ CKD
□ K Sparing Diuretics
□ Addison’s Disease

Question 17

Redistribution of K –

how does acidemia lead to hyperK

How does eating a high carb meal lead to hyperK; what is the consequence?

Answer 17

□ Acidemia – in high acid states, body tries to Hide H+ in RBCs, which then pushes out K +

□ Hyperkalemia Periodic Paralysis – patients after high carb meal, lots of K leaves the cells, and leads to a paralysis

Question 18

Clinical conseuqnces of HyperK

Answer 18

§ Cardiac – EKG changes — MEDICAL EMERGENCY; the myocardium is irritable and lead to automaticity; vtach and vfib

□ Peaked T waves
□ Prolongation of QRS
□ Death

Question 19

Treatment of Hyperkalemia –

Temporizing solution –

Lasting Solution

Answer 19

Temporizing solution – § Antagonize the Cell membrane – bringing the RMP back to a normal level (give Calcium, Hypertonic Saline)

Removal of the K
1) Diuretics – pee it out (but HyperK is usually in CKD pts)

2) K Exchange Resins – osmitic agent pulling K via the gut
3) Dialysis