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Lesson: 32. Potassium balance disorders.
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BY PAUL GEDEON

Potassium balance disorders.

Physiological function of K  • Mostly intracellular (98%)

  • Uses:
    • Protein and glycogen synthesis
    • Neurotransmission (determines membrane potential: ratio of intra:extracellular)
  • K balance regulated by:
    • K+ uptake by cells (transcellular distribution) via Na/K ATPase, stimulated by insulin and beta 2 agonists.
    • Urinary K excretion via :
      • Aldosterone stimulating Na/K ATPase @ basolateral + other channels on apical
      • Increased distal flow to CCT = more K excretion
    • Renal handling:
      • Extensively reabsorbed in proximal tubule and TAL o Excretion via aldosterone in CCT

Role in membrane potential

  • Ratio of EC/IC determines resting potential
  • Increased EC (hyperK) = raises resting potential since EC:IC ratio is increased I.e relatively lower IC K+ means moving away from K+ membrane potential of –90mV (depolarises)
  • Decreased EC (hypoK) = lower resting potential (Makes it more negative) since EC/IC ratio is decreased I.e relatively the IC K+ is higher, moving the RP towards more negative (hyperpolarises)
  • Both will end up in flaccid paralysis. HyperK first results in depolarisation and contraction but then membrane becomes unresponsive and you get flaccid paralysis.

Low potassium (3 situations) < 3.5mmol/L

Normal body stores

  • HypoK due to EC to IC shift
  • Causes:
    • Insulin admin
    • Catecholamines (coffee or therapy)
    • Cellular compensation in alkalosis (H+ moved out of cell and K+ moved in ) o Treating pernicious anemia (lots of new cells, rapidly taking up a lot of K+). Tumor cell formation hypoK via same mech.

K+ depletion without without hypoK (IC depletion)

  • Severe renal failure
  • DKA
  • Congestive heart failure

Depleted body stores with hypoK

  • HypoK due to an actual decrease in the total body K+ amount.
  • Causes o Poor K+ intake in alcoholism and anorexia nervosa
    • Burns: Skin loss of K+ o GI K+ loss:
      • In HCl loss (e.g vomiting) = metabolic alkalosis –> maintenance by volume depletion (see acid-base lectures) –> renal K+ wasting
  • Diarrhea, enemas, uretero-sigmoidostomy (acid-base lecture) o Renal K+ loss (losing >40mmol/day)

Signs of hypok

  • Neuromuscular o Fatigue
    • Skeletal and respiratory muscle weakness o Constipation o Ileus
  • ECG o Long PR
    • Increased QRS amplitude and width o ST depression o Flat/inverted T  o Prominent U wave
    • Arrhythmias! (VT, VF, Torsades)

Hyperkalemia > 5.1 mmol/L

Hyperkalemia with normal total body K

  • In-vitro = pseudohypokalemia due to hemolysis, thrombocytosis and leukocytosis
  • IC to EC shift o Exercise
    • Lack of insulin (DM hyperglycemia) o Cell destruction
    • Acidosis: H+ shifted into cell and K+ shifted out of cell

Hyperkalemia with elevated total body K+

  • Increased K+ load o Dietary salt supps (KCl) o Iatrogenic
  • Decreased renal K+ excretion o Lowered GFR (renal failure) = decreased distal flow = decreased secretion
    • Reduced tubular secretion in hypoaldosteronism
      • RTA-4
      • Addison’s
      • ACE-inhibitors o Renal transplant, urinary tract obstruction

Signs of hyperK

    • Neuromuscular = paresthesia, muscle weakness, flaccid paralysis
    • ECG
      • Flat or absent P wave o Wide sine-wave-like QRS  o ST elevation or depression
      • Peaked, tall T waves (II, III, V2-V4) or T wave > R wave
    • Death if K+ > 8 mmol/L because of VF, asystole

 
 
 
 
 
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