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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