Hypokalamia/Hyperkalemia Flashcards

1
Q

potassium predominantes in what fluid compartment?

A
  • most common cation in the ICF (whereas sodium is the most common cation in the in the ECF)
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2
Q

what is the effect of insulin on [K+] in the ICF/ECF?

A

insulin directly pumps K+ into cells, maintaining the high intracellular [K+]. this in turn stimulates the Na+/H+ antirpoter, promoting H+ secretion

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3
Q

which patients should regularly have their potassium checked?

A
  • patients with cardiac disease
    • both hypo/hyper - kalemia could have significant effects on cardiac conduction
    • K+ levels are critically important in patients with an MI, dysthrythmias, or receiving digoxin therapy
  • patients receiving drugs that may effect K+ level
    • risk of hypokalemia - by loop diuretics
    • risk of hyperkalemia, with
      • k+ sparing diuretics
      • ACE inhibitors
      • NSAIDS
  • patients with diabetes mellitus
    • acute DKA
    • type IV renal tubular acidosis
  • patients with major fluid/electrolytice imbalances
    • those on IV fliuds
    • those receiving parenteral nutrition
    • tthose w/ severe diarhea
  • patients with renal impairments
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4
Q

what serum [K+] levels constitute hyperkalemia?

A

a serum [K+] > 5.5 mEq/L

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5
Q

what to look out for during a physical exam a possibly hyperkalemic patient?

A
  • exam will usually be negative
  • otherwise, you may see
    • bradycardia
    • weakness, fatigue
    • dyspnea
    • arrthymias
    • parethesias
    • nausea and vomitting
    • muscle tenderness/weakness/paralysis
    • depressed or absent deep tendon reflexes
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6
Q

discuss the pathophsyiology (common causes) of hyperkalemia?

A
  • excessive intake of K+ (rare)
  • decreased excretion of K+ (almost all of these causes involved decrease in aldosterone)
    • kidney disease (chronic or acute)
    • Addison’s disease:
      • characterized by a decrease in aldosterone production: less Na+ absorbed, less K+ secreted at collecting ducts –> K+ retention
    • Type IV RTA (Renal Tubular Acidosis)
      • this variation of RTA is due to an aldosterone deficiency.
      • K+ retention drives K+ out of the plasma in the cell. this promotes uptake reabsoprtion of H+ in “exchange for” the K+ we’re trying to get rid of
    • drugs:
      • diuretics that lower K+ secretion:
        • potassium sparing diruetics
        • ACEs/ARBS
          • (these lower inhibit Ang II and thus aldosterone production)
      • renin inhibitors
        • ​RAAS decrease –> aldosterone decrease –> K+ retention
  • a shift of K+ from intracellular to the extracellular space
    • rhabdomyolsis - muscle breakdown
    • hemolysis - breakdown of RBCs
    • metabolic acidosis
    • drugs: beta blockers and alpha antagonists
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7
Q

clinical presentation of rhabdomyolysis

A
  • rhabdomyolysis = muscle breakdown that causes a causes a shift of K+ from the ICF to the ECF
  • presentation:
    • myalgias
    • dark urine
    • possible compartment syndrome
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8
Q

discuss the EKG changes seen in hyperkalemia

A

different EKG changes are seen dependent on the level of hyperkalemia (serum K+ > 5 mEq/L)

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9
Q

how to check renal function for a hyperkalemic patient?

A
  • determine the BUN and Creatinine
    • creatinine clearance = used to estimate GFR
      • can estimate creatinine clearance using the Cockcroft- Gault Formula (utilizes patient’s age and body weight)
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10
Q

what can urine potassium levels you with regards to hyperkalemia?

how to obtain these urine levels?

A
  • A urine K+ level <20 mEq/L suggests impaired renal excretion
  • A urine K+ level > 40 mEq/L suggests intact renal excretory mechanisms
    • means that hyperkalemia is likely nonrenal

a spot urine K+ measurement is easiest to obtain

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11
Q

outline the diagnosis of hyperkalemia based on serum [K+], luekocyte/platelet levels, and urine [K+]

A
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12
Q

general treatment of hyperkalemia?

A
  • Discontinue all drugs causing hyperkalemia (K+ sparing diruetics -spironlactone, eplernone, triamterine, amiloride - and trimethoprim)
  • Discontinue any dietary potassium
  • If pt on digoxin, check for digitalis toxicity—Hyperkalemia
    • In severe (potassium >7.0 mEq/L) OR if pt is symptomatic
      • Start treatment first!
      • Then look for underlying cause

in pharm, digoxin is contraindicated with loop/thiazide diuretics because it can “worsen hypokalemia” idk what to do about this.

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13
Q

after intitial treatment for hyperkalamia (discotinuing K+ retaining drugs, ect.) what is the next step?

A
  • next step is achieving membrane stabilization
    • calcium is key in stabilizing membrane stability (use either calcium chloride or calcium gluconate)
  • next, want to drive K+ intracellullary:
    • this is often done with insulin, which drives K+ into cells.
      • if insulin is give, also administer glucose so pt doesnt beome hypoglycemic.
    • this can also be done with:
      • bicarbonate (especially if the patient is also acidotic)
      • magnesium
      • sympathonimetic agents (eg beta-agonists)
  • we can also remove K+ from the body entirely:
    • hemodialysis
    • normal saline
    • furosemide (loop diuretic)
      • remember that loop diuretics increase the tubular Na+ load that arrives to the collecting ducts, which then drives Na+ reabsorption/K+ secretion
        • this promotes excretion of K+
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14
Q

what blood serum is considered hypokalemia?

A

serum level < 3.5 mEq/L

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15
Q

general causes of hypokalemia

A
  • inadequate potassium intake
  • increased potassium excretion (most common)
  • shft of potassium from ECF to ICF
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16
Q

clinical presentation of hypokalemia

A
  • is identical to that of hyperkalemia. thus, clinical presentation alone is not enough to diagnose hypokalemia
    • generally, is asympotomatic
    • if symptomatic
      • weakness and fatigue*
      • muscle cramps
      • palpitations
      • worsening polyuria
      • psychosis, hallucinations
17
Q

what labs/serum levels should you obtain to diagnose hypokalemia?

A
  • BMP/CMP
  • magnesium assay
  • ECG
  • urine potassium
18
Q

what should we check to determine if a patient’s hypokelemia is due to extrerenal vs renal causes?

A

check urine K+

  • if urine K+ is <20mEq/L, consider extrarenal causes
  • if urine K+ is >20mEq/L, consider renal losses
19
Q

what are the common extrenal causes of hypokalemia?

A
  • GI causes: diarrhea
  • Use of laxatives, insulin, etc
  • Low potassium intake (uncommon)
20
Q

what renal losses would cause hypokalemia?

A

HTN + alkalosis—-check aldosterone (check aldosterone b/c increased aldosterone would cause both HTN & K+ loss:

  • Low aldo/ low renin: issue is increased cortisol: Cushing’s syndrome, Liddle’ ssyndrome
  • High aldo/low renin: Primary aldosteronism
  • High aldo/high renin: Secondary hyperaldosteronism

Normal/low BP or low—check acid-base

  • Acidosis: Renal tubular acidosis 1 or 2
  • Alkalosis: diuretics ,vomiting, Bartters yndrome, Gitelman syndrome
21
Q
  • bartter syndrome causes what kind of hypokelmia?
  • how does it present?
A
  • causes hypokelamia via renal losses: (Uk > 20 mEq/L)
    • _​_urinary loss oss of Na+, Cl+, K+
    • presents with metabolic alkalosis WITHOUT HTN**
    • other things: hypochloremia, hyoreninemia
22
Q

gitelman syndrome

  • what kind of hypokelemia does it cause?
  • how does it present?
A
  • causes hypokalemia due to renal losses (Uk > 20 mEq/L)
  • presents with meatbolic alkalosis WITHOUT HTN - normal or low BP
  • other things: hypokalmia, hypomagnesia, hypocalciuria
23
Q

what ECG changes are seen with hypokalemia?

A
  • ST depression
  • prominent U wave
24
Q

what arrythmias can result from hypokalemia?

A
  • ventricular arrythmias
    • torsades de point
      • in this case, hypokalmia will be seen along with hypomagnesemia
    • ventricular tachycardia
25
Q

what are the three general steps we want to take when treating hypokalemia?

A
  • reduce K+ losses
  • replenish K+ stores
  • correct Mg++
26
Q

how do we reduce K+ losses when treating hypokalemia?

A
  • discontinue
    • loop/thiazide diruetics
      • if pt needs a diuretic, put them on a K+ sparing diuretic
    • laxatives
  • treat diarrhea/vomitting if needed
27
Q

how do we replenish K+ stores when treating hypokalemia?

A

by supplying K+

  • if K+ level 2.5-3.5 mEq/L: may only need oral potassium replacement
  • if K+ level <2.5 mEq/L: they need IV potassium
    • for these patients, continuously monitor ECG
28
Q

when treating hypokalemia: after reducing K+ losses and replenishing K+ stores, what must we do next?

A

correct Mg+. bring Mg+ back to a normal level

29
Q

discuss the relationship between Mg+ levels and hypokalemia. what does this mean clinically?

A
  • Mg depletion can cause potassium depletion
    • mechanism poorly understood: something to do with Mg+ loss impairing the ability of cell to maintain K+ (normally ECF [K+] very high)
  • this means that repletion of cell potassium requires correction of magnesium deficit
30
Q

outline steps for determining cause of hypokalemia

A
31
Q
A