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Primary Impression

Primary Impression. Hypokalemia secondary to Primary Aldosteronism (Conn’s Syndrome). Why rule in Hypokalemia?. Acute Generalized weakness Absence of UMN and LMN signs, Sensory and Autonomic Involvement, Bulbar signs and Fatigability. Marked decrease in K+ level (1.5mmol/L).

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Primary Impression

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  1. Primary Impression • Hypokalemia secondary to Primary Aldosteronism (Conn’s Syndrome)

  2. Why rule in Hypokalemia? • Acute Generalized weakness • Absence of UMN and LMN signs, Sensory and Autonomic Involvement, Bulbar signs and Fatigability. • Marked decrease in K+ level (1.5mmol/L)

  3. Definition of Hypokalemia • Plasma K+ concentration <3.5 mmol/L • May be due to: • Decreased net intake • Shift of K+ into cells • Increased net loss

  4. Clinical Manifestations of Hypokalemia • Usually asymptomatic • Unless plasma K+ concentration <3 mmol/L • Fatigue, myalgia, muscular weakness of the lower extremities • Severe Hypokalemia → progressive weakness, hypoventilation and complete paralysis

  5. Occurrence of Metabolic Alkalosis • High pH (7.56) • Low pCO2 (32) • High HCO3 (28.7) • Result of K+ redistribution + excessive renal K+ loss • K+ depletion → intracellular acidification →increase HCO3 production

  6. Primary Hyperaldosteronism (Conn’s Syndrome)

  7. Why rule in Primary Hyperaldosteronism? • Triad of Hypertension, Hypokalemia, and Metabolic Acidosis • Elevated BP upon admission • Diagnosed with HTN 7 years ago • Poor compliance to maintenance medications • Hypokalemia and Metabolic Acidosis on lab tests

  8. Primary Hyperaldosteronism • Syndrome associated with hypersecretion of adrenal mineralocorticoid Aldosterone • Accounts for 5-10% of hypertension cases • Peak incidence → 30-60 years old

  9. Pathophysiology • Cellular uptake of K+ • Aldosterone → inc. Na+-K+ ATPase] → inc. transport of K+ into intracellular space • Regulation of Renal K+ transport • Aldosterone →inc. Apical Na conductance, basolateral Na+-K+ ATPase activity, and electrogenic Na absorption in the collecting tubules → K+ movement from intracellular to luminal fluid

  10. Excessive aldosterone • increased sodium retention • decreased plasma renin • Increased renal potassium excretion →hypokalemia

  11. Clinical Manifestations • Hypokalemia • Muscular weakness • K+ depletion in the muscle cell membrane • Paresthesias • Headache • Polyuria • Polydipsia • Moderate hypertension (diastolic) • Due to inc. Na reabsorption

  12. Plasma Renin Activity (PRA) Plasma Aldosterone Concentration (PAC) • Primary Hyperaldosteronism is consistent with: • ↓PRA (baseline-12.69 ng/dL; post-12.36 ng/dL) • ↑PAC (<0.1 ng/mL/hr),

  13. Diagnostics • CT Scan

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