pour Cliquez modifier le style des sous-titres du masque NURS 324 Fall 2010 Dr. Smith
Diuretics Fluid and Electrolyte
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Renal A&P Review
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Structure/Function of Nephrons
Three Main Processes -filtration (at glomerulus) -reabsorption (PCT, Henle loop, DCT) -secretion (PCT)
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Formation of Urine
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Diuretics
All types share the same basic MOA: blockage of Na and Cl reabsorption -reduced Na/Cl reabsorption also blocks H20 reabsorption The effect on urine production is directly related to the amount of Na/ Cl reabsorption that a diuretic blocks
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Diuretics
General Uses: -treatment of hypertension -edema related to heart, renal, or liver failure General Adverse Effects: -hypovolemia -acid/base imbalances -other electrolyte imbalances
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Categories
Loops high-ceiling Thiazides Osmotics Potassium-sparing (aldosterone antagonists and nonaldosterone antagonists) Effectiveness of each type depends upon its site of action in the kidney
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Sites of Action of Diuretics
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Loop Prototype: Furosemide (Lasix)
MOA: blocks Na/Cl reabsorption in the thick segment of ascending Loop of Henle Produces significant diuresis Used when significant fluid excess exists: pulmonary edema r/t CHF, edema or HTN untreated by other diuretics Furosemide can be effective even
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Furosemide (Lasix)
Hypotension Adverse Effects Administration/A Pharmacokinetic bsorption s
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Furosemide (Lasix) Interactions
Digoxin risk of dig toxicity in people who are hypokalemic Ototoxic drugs Potassium-sparing diuretics
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Thiazides
MOA: block Na/Cl reabsorption in the early DCT Main difference is they cause less diuresis than loops Only effective with an adequate GFR Uses: essential HTN, moderate edema -zides
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Thiazide Prototype: Hydrochlorothiazide (HCTZ)
Hyponatremia, Adverse Effects Administration/A Pharmacokinetic h bsorption s ypochloremia,
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Potassium-Sparing Diuretics
General effect: retention of K and excretion of Na in the distal nephron Used mainly for potassium-sparing actions; cause minimal diuresis Adverse effect: hyperkalemia Two categories
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Potassium-Sparing Diuretics
Nonaldosterone Prototype: Aldosterone triamterene S ntagonists Apironolactone
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Osmotic Diuretics
MOA: create an osmotic force within the nephron, preventing reabsorption of some water Uses: prevention of renal failure, reduction of ICP and IOP (draws fluid out of cerebral tissue and ocular tissue)
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Osmotic Prototype: Mannitol
Edema (except Adverse Effects Administration/A Pharmacokinetic in bsorption s the brain,
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Disorders of Fluid Balance
Volume contraction = decreased body water Volume expansion = increased body water Contraction/expansion can be isotonic, hypertonic, or hypotonic Isotonic = equal amounts of fluids & electrolytes are lost/gained Hypertonic = left with hypernatremia
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Treatment of Fluid Imbalances
Isotonic treat contraction: with isotonic fluids, slowly to avoid pulmonary edema Hypertonic contraction: treat with PO water if moderate, hypotonic fluids if severe, done in stages Hypotonic contraction: if mild and kidneys OK, give IV isotonic fluids. If severe, give hypertonic fluids up to Na = 130 mEq/L 2/16/11
Ion (pH) Imbalances
Respiratory alkalosis/acidosis: generally treat by fixing respiratory problem Metabolic alkalosis: infuse NaCl + KCl, this causes renal excretion of HCO3-if severe, may need infusion of dilute HCl (central line only!) Metabolic acidosis: correct
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Potassium Imbalances
Potassium levels are affected by ECF pH -ECF alkalosis enhances K uptake by cells -ECF acidosis enhances K kick-out by cells Potassium levels also affected by insulin: high levels stimulate K uptake by cells
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Treatment of Hypokalemia
Oral KCl: several formulations, differ by speed of release -may have adverse GI effects, take with plenty of water IV KCl: must give diluted and slow, can be very irritating to veins -check K levels periodically to avoid hyperkalemia
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Treatment of Hyperkalemia
First, withhold K-rich foods or supplements Next, infusion of insulin and glucose If also acidotic, sodium bicarbonate will correct pH and encourage K uptake by cells Finally, can directly remove K -Kayexalate absorbs K into stool -dialysis
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The Renin-AngiotensinAldosterone System
Renin is produced and released by the kidneys in response to decreased BP, volume, renal perfusion pressure Renin converts angiotensinogen to angiotensin I ACE converts angiotensin I to angiotensin II Kinase II (same chemical, different name) also metabolizes bradykinin
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Effects of Angiotensin II and Aldosterone
Angiotensin II -powerful vasoconstriction (direct & indirect) -promotes aldosterone release -cardiac hypertrophy and remodeling -thickening of blood vessel walls Aldosterone -retention of Na and H20 in kidneys -cardiac remodeling?
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ACE Inhibitors (ACEIs)
MOA: blocks activity of ACE, thereby reducing levels of angiotensin II and increasing bradykinin levels Uses: -hypertension -heart failure (vasodilation -> decreased work) -reduce mortality after an MI -delay or slowing of nephropathy
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ACEI Prototype: Ramipril (Altace)
First-dose Adverse Effects Administration/A Pharmacokinetic h bsorption s ypotension
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ACEI Interactions
Diuretics Other hypertension drugs Potassium supplements or potassium-sparing diuretics
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Angiotensin II Receptor Blockers
MOA: block the receptors for angiotensin II, causing essentially the same effect as ACEIs Difference is the lack of effect on kinase II, which reduces some of adverse effects Uses: all approved for HTN various ones, but not all, are approved for heart failure, diabetic
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ARB Prototype: Losartan (Cozaar)
Angioedema Adverse Effects Administration/A Pharmacokinetic bsorption s Teratogen
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