Disorders of Potassium Metabolism Flashcards Preview

Renal Block > Disorders of Potassium Metabolism > Flashcards

Flashcards in Disorders of Potassium Metabolism Deck (11):
1

1. Appreciate the role of potassium (major intracellular cation) in maintaining cell integrity, especially within the neuromuscular and cardiac systems.

98% of K is located intracellularly, because it influences cell membrane potential, it is regulated within a narrow window 3.5-5mmol/L by regulating GI absorption and renal excretion

intracellularly, potassium is important for protein synthesis, cell growth, and in influencing cell membrane potential

intra and extra cellular levels of K+ effect the resting potential and may make the cell more or less likely to reach threshold and propagate an AP; results in disrupted neuron/cardiac conductivity and weakness/paralysis of skeletal muscle

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2. Describe the mechanisms the maintain potassium homeostasis speaking systemically (absorption, excretion and cellular intake)

intake of 60-150 mmol/day of which 90-95% is absorbed in GI tract
output of 90% lost in urine and 10% lost in stool

cellular uptake is a major way to "temporize" total body levels which is managed by a Na/K ATPase for uptake

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3. List and describe factors that lead to hypokalemia, including both kidney and non-kidney mechanisms with particular attention to potassium wasting and retention.

decreased dietary intake (alcoholism, anorexia)

increased K+ uptake into cells caused by:
(high K+ plasma K+ in normal conditions)
insulin release
catecholamines
aldosterone
alkaline pH of blood/interstitial
anabolic activity (H+ production within cell)

increased secretion with increased aldosterone, high tubular flow/Na delivery or negative charges in the lumen
diuretics inhibit sodium and chloride reabsorption (block NKCC channel) (Bartter's Syndrome); increased delivery of Na to distal nephron can enhance K+ secretion (Gittelman Syndrome)

increased stool loss (diarrhea- aldosterone in low volume state, laxative)
vomiting: low volume/aldosterone and metabolic alkalosis

hyperaldosteronism due to adrenal adenoma causes hypokalemia; can be secondary due to RA stenosis, RAAS increase

aldosterone promotes decrease K+ and K+ travels in opposite direction of H+ in cells and tubules)

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3. List and describe factors that lead to hyperkalemia including both kidney and non-kidney mechanisms with particular attention to potassium wasting and retention.

increased intake, particularly with IV replacement

transcellular shift out of cells:
tissue breakdown
acidotic pH (blood/ interstitial)
insulin deficiency (DM I)
use of B-Blockers
(low plasma potassium under normal conditions)

decreased K+ secretion: decreased aldosterone (Addison's), low tubular flow (AKI or CKD) or inability to filter/compensate and regulate levels, low Na delivery (DM nephropathy), RAAS impairment (ACEI, spirolactone), and other meds (NSAIDs, potassium sparing diuretics: traimterene and amiloride block ENaC)

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4. Explain the pathophysiologic effects of potassium deficiency on neuromuscular, cardiac, metabolic function and kidney function.

hypokalemia (<3.5 mmol/L) can cause hyperpolarization and increased threshold for AP

results in fatigue, malaise, myalgia (in severe cases: paralysis and rhabdomyolysis

EKG may show higher threshold, delayed repolarization of the ventricle (resulting in U wave) and PVCs, Vtach or Vfib

low K+ inhibits insulin release leading to high glucose levels

Note: K+ is needed during exercise to maintain vasodilation to avoid muscle ischemia

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4. Explain the pathophysiologic effects of potassium excess on neuromuscular, cardiac and kidney function.

enhanced depolarization and delays in depolarization in the neuromuscular junction causes skeletal muscle weakness and paralysis (sub threshold depolarization causes activation of sodium channels, loss of excitability

hyperkalemia can caused sustained sub threshold depolarization leading to delayed depolarization, EKG changes (enhanced depolarization causes peaked T wave along with delated atrial and ventricualr depolarization), arrhythmia and death

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5. Describe the three categories of etiologies of hyperkalemia.

increase intake
decreased output
cell break down

note: lysis of cells in blood sample can lead to pseudo hyperkalemia

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6. Recognize hyperkalemia clinical, acknowledges signs and symptoms apparent.

muscle weakness
paralysis
arrhythmias
death

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7. Explain the different treatments for hypokalemia an dhow and when to use specific treatments.

treat underlying illness
eliminate dietary restriction
add dietary supplementation (mild hypokalemia)
oral or IV replacement (moderate hypokalemia)

avoid further bicarb admin
hypercholemic metabolic acidosis tx. with K citrate or Kbicarb

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7. Explain the different treatments for hyperkalemia an dhow and when to use specific treatments.

1. restore excitability of cardiac myocytes: Ca gluconate or CaCl2 antagonize the effects of potassium

2. Shift potassium into ICF with insulin, sodium bicarb, B2 agonists

3. removal via stool or urine: stool (sodium polystyrene and sorbitol); urine (enhance urine output or dialysis)

11

2. Describe the mechanisms the maintain potassium homeostasis speaking specifically about controls in the kidney.

potassium is freely filtered (100%)

65% is reabsorb in the PCT, 25% in the thick ascending limb, reabsorption in the PCT is mostly paracellularly ("passive transport"), reabsorption in the thick ascending limb is via NKCC symporter with the active reabsorption of Na (causes charge gradient)

10-20% secretion blood to tubule by the principle cells of the collecting ducts via ENac channels