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8 Cards in this Set

  • Front
  • Back

Cortical Collecting Tubule

-Principle Cells: Regulate Na+/H2O reabsorption via ENaC


-Intercalated cells: Control Acid/Base balance via Bicarbonate absorption. Response to Aldosterone


-Principal Apical: ENaC (Na+ in, K+ out) Amiloride


-Basolateral: ATPase (NA+/K+)


-CCT, target of K+ sparing diuretics

Aldosterone

-mineralocorticoid (steroid hormone)


-Secreted by adrenals


-Increase ATPase (Na+/K+ basolateral side)


-Increases Na+/H2O reabsorbtion


-Addison's Disease: Aldosterone deficiency

ADH or Arginine Vasopressin

-Vasoactiv peptide secreted by posterior pituitary


-Activates ADH receptor on Vasculature


-Constricts Periph Vasculature


-Promotes Water Reabsorption in CCT


-CCT not water permeable w/o ADH


Loop Diuretics/Thiazide Waste K+

-Increase Na+ deliver to CCT increases secretion of K+ and H+ by CCT


-Hypokalemic Metabolic Alkylosis


-K+ loss

Potassium Sparing Diuretics -Amiloride

-Direct inhibitor of ENaC


-Preserve cardiac function


-Prevent HF


-Hyperkalemia


-Acidosis

Potassium Sparing Diuretics -Spironolactone

-Synthetic steroid -->interferes w/ aldosterone


-Reduces Na+ reabsorption by reducing ATPase expression


-Prevent HF


-Preserve Cardiac function


-Hyperkalemia


-Acidosis


-Gynecomastia

ADH receptor agonists -Vasopressin/Desmopressin

-Act as antidiuretic just like ADH


-Treat pituitary diabetes insipidus


-Toxic: monitor for water toxicity

ADH receptor antagonists - Conivaptan

-Inhibits vasopressin ADH


-Hypertension


-HF


-Counteract high ADH in SIADH


-Infusion site reactions/hypernatremia