by mtoom

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What is the normal serum [K+]?
3.5 - 5.0 mEq/L
Where is 98% of K+ found?
Intracellular fluid (ICF)
What role does K+ play in the cell as an electrolyte?
Most abundant cation
Why is the balance of high [K+] inside the cell and low [K+] outside the cell so important?
It is critical for normal cell membrane potential (and thus nerve conduction and muscle contraction)
What maintains the intracellular and extracellular [K+] concentrations?
Na+/K+ pump
What 2 drugs will stimulate the Na+/K+ pump to drive K+ into the cell?
  • Insulin
  • β-adrenergic catecholamines
  • What is the average dietary intake of K+?
  • How much K+ needs to be excreted to maintain total body potassium balance?
  • How much K+ is excreted by the kidneys?
  • 60-150 mEq/day
  • The amount in diet is what needs to be excreted to maintain balance
  • Excretion is 95% kidney (5% stool/sweat)
  • How much K+ is filtered?
  • Name 2 places K+ is reabsorbed, and how much is reabsorbed.
  • What is the main site of K+ secretion, and what is the primary regulator of K+ secretion?
  • K+ is freely filtered
  • Reabsorption:
    PCT (65-75%)
    TAL (15-25%) by Na/K/2Cl
  • Secreted in CCD, aldosterone is the primary regulator
Describe 4 factors that determine secretion of K+
  • Aldosterone (upregulates Na+/K+ exchange)
  • Tubular Luminal Flow
  • Delivery of luminal Na+ (increases Na+/K+ exchange, this effect is seen in diuretics)
  • Acid-base (in acidosis, H+ may be secreted in place of K+)
What are the effects (5) of Aldosterone on the principal cells of the CCD, and the lumen at the CCD?
  • Aldosterone activates existing ENaCs (Epithelial Na+ Channel)
  • Aldosterone activates Na+/K+ pump (necessary to drive Na+ reabsorption)
  • Aldosterone causes creation and insertion of new ENaCs
  • Aldosterone creates a more electronegative lumen (by driving Na+ more reabsorption, Cl- is left behind causing an electronegative lumen)
  • Aldosterone causes increased secretion of H+ (by having created the more electronegative lumen; this is one of the mechanisms of perpetuating metabolic alkalosis)
How does increasing the luminal flow of K+ affect the K+ secretion?
Increases in flow rate enhances K+ secretion
What happens after a meal when serum [K+] rises (2)?
  • Insulin and catecholamines cause cells to take in more K+
  • Aldosterone is released, acting on CCD to increase K+ secretion (more K+ is excreted in urine)
Remember: The amount of K+ excreted is equal to the amount of K+ ingested, maintaing K+ balance
What is Trans-Tubular Potassium Gradient (TTKG)?
It is basically the ratio of urine K+ to blood K+ divided by the ratio of the osmolality in urine and blood.

TTKG estimates the lumen [K+] relative to the blood [K+].

It is higher when aldosterone is high (because aldosterone stimulates Na+/K+ exchange at the CCD).
What is the definition of Hyperkalemia?

When is the [K+] dangerous?
  • Hyperkalemia: > 5.0 mEq/L
  • Dangerous: > 6.0 mEq/L
Give 3 reasons why Hyperkalemia might occur.
  • Increased K+ intake/GI load (note: this is a very unusual cause of hyperkalemia if kidney is functioning properly)
  • Impaired renal excertion
  • Shift of K+ out of cells (from ICF to ECF)
Give 7 examples of things that can cause a shift/redistribution of K+ from ICF to ECF
  • Insulin deficiency (diabetic, catabolic state)
  • β-adrenergic blockers
  • Metabolic acidosis (ICF is buffering the H+ by exchanging it for K+)
  • Digoxin toxicity
  • Cell breakdown (eg. rhabdomyolysis, tumor lysis, hemolysis)
  • Increased osmolality (eg. hyperglycemia)
  • Hyperkalemia periodic paralysis
Name 2 main causes of decreased excretion of K+
  • Decreased GFR
  • Impaired secretion
Name 2 causes of decreased GFR that can contribute to excretion of K+
  • Acute/chronic renal failure
  • Volume depletion (resulting in decreased luminal flow, decreased Na+ delivery)
Name 2 causes of impaired secretion of K+and give examples
  • Decreased aldosterone (Adrenal insufficiency, Addisons, NSAIDS)
  • Drugs (K+-sparing diuretics, spironolactone, ACE-inhibitors under some circumstances, ARBs)
When is hyperkalemia imminently dangerous?

How do you treat it?
  • If >6.5 mEq/L or ECG changes, treat hyperkalemia right away
  • Then, determine and correct underlying cause
You would give IV calcium to antogonize the effects of the hyperkalemia on the heart.
Name 2 ways to treat hyperkalemia by moving K+ into ICF?
  • Insulin + Glucose (preferred)
  • β-agonist
Name 3 ways to treat hyperkalemia by removing K+ from the body?
  • GI excretion (eg. exchange resins, PO or enema)
  • Renal excretion (eg. loop diuretics)
  • Hemodialysis
What is another exogenous cause of hyperkalemia that can be corrected?
Offending medications (eg. ARBs, K+ supplements, etc.)

These should be stopped.
What concentration is hypokalemia?

What concentration of K+ is life-threatening?
  • Hypokalemia: K+ less than 3.5 mEq/L
  • Life-threatening hypokalemia: K+ less than 2.5 mEq/L
What are 2 symptoms of hypokalemia?
  • Muscle weakness
  • Cardiac arrythmias
What drug can potentiate the cardiac effects of hypokalemia?
Describe a mechanism for hypokalemia (3 steps)
  • Decreased intake K+
  • Increased shift from ICF to ECF
  • Increased losses (GI, renal)
With respect to etiology of Hypokalemia, describe:
  • Dietary cause (1)
  • Increased shift from ECF to ICF (5)
  • Increased loss (2)
  • Decreased dietary intake (less than 25 mEq/day)
  • ECF to ICF shift: Beta-agonists, insulin, refeeding, alkalosis, hypokalemic periodic paralysis
  • Loss by GI tract (diarrhea, laxatives)
  • Loss by Renal (diuretics, vomiting, NG suction, hyperaldosteronism, increased exogenous mineralocorticoids, rental tubular defects, drugs)
How do you treat Hypokalemia?
  • Severe; cardiac monitor
  • Check Mg level & replace
  • Check if on Digoxin
  • Rapidly replace K+ (IV, or PO);
    replace total body deficit slowly
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