Flashcards in diuretics Deck (30)
what are forces that favor filtration?
-glomerular hydrostatic pressure 60 mmHg (pushing out)
-bowman's capsule colloid osmotic pressure of 0 (pulling in)
what are forces that oppose filtration?
bowman's capsule hydrostatic pressure 18 mmHg (pushing against)
glomerular capillary osmotic pressure 32 mmHg (pulling in)
what is the net filtration pressure in the glomerular capsule?
what is the best way to increase urine output?
increase perfusion to kidneys by increasing BP, which increases filtration pressure
how is GFR normally preserved?
autoregulation: maintaining constant RBF over a range of systemic BP with MAP 50-150 mmHg
*HTN pts. have higher GFR when RBF is constant
*CHF pts. have decreased RBF and GFR
-myogenic: increased arterial pressure stretches afferent arteriolar wall then a reflex constriction occurs; decreased arterial pressure causes arteriolar dilation
-tubuloglomerular: decreased RBF leads to decreased GFR which results in afferent arteriolar dilation which increases GFR and RBF and restores filtration
-renin released, causes conversion of angiotensin I into II (aldosterone follows angiontensin II as well) causing vasoconstriction and increased GFR
what makes up urine besides water?
-electrolytes: primarily sodium, potassium, chloride, and bicarbinates
-waste products: creatinine
what determines urine excretion rate?
filtration rate - reabsorption rate + secretion rate
what are uses for diuretics?
-reduce HTN (decrease intravascular fld. vol.)
-treat pulmonary and peripheral edema
-electrolyte and pH corrections (hyperkalemia)
-reduce ICP, brain bulk
-prevent ARF d/t ischemic insult
which drugs are loop diuretics?
-ethacrynic Acid (Edecrin)
what is the MOA of loop diuretics?
inhibit reabsorption of NaCl in ascending loop of Henle
-stimulate production of prostaglandins (vasodilation, increased RBF)
*non increase in GFR
describe loop diuretics
-used more to decrease intravascular fld. vol.
-most effective diuretic class
-works faster than thiazide diuretics
-rapid excretion of drugs (used in ER for OD pts.)
what are some clinical uses of loop diuretics?
-rapid intravascular fld. removal
-acute pulmonary edema
-kidney stone extraction, lithotripsy
-reduce intracranial pressure (systemic diuresis and decreased CSF production; used w/ mannitol)
what are concerns with loop diuretics?
-hypokalemia (potentiates digitalis toxicity; enhances NMB)
-ototoxic (permanent or transient deafness
-potassium replacement may be needed
-cardiac dysrhythmias can occur
-fld. vol. replacement may be indicated (orthostatic hypotension, hemoconcentration like increased BUN, Hct)
what drugs are thiazide diuretics?
-hydrochlorothiazide (Microzide, Esidrix)
what is the MOA of thiazide diuretics?
-inhibits reabsorption of NaCl in loop, proximal and distal tubules
-decrease HTN by diuresis, vasodilation (SNS in peripheral vascular smooth muscle d/t decreased total body stores of Na+
-excretion of Na+, Cl-, Bicarb, Mg++ and ultimately K+
what are clinical uses of thiazide diuretics?
-reduces edema (edema from CHF)
-reduces intravascular fld. vol (HTN)
*used in combination with antihypertensive drugs
what are effects of thiazide diuretics?
-decreased K+, Mag++, Cl-
-hypochloremic metabolic alkalosis
-hyperuricemia (gouty arthritis)
-hypokalemia (potential for digitalis toxicity, cardiac dysrhythmias, muscle weakness, neuropathy, enhance NMB)
*potassium replacement may be indicated
*fld. vol. replacement may be indicated (orthostatic hypotension, hemoconcentration)
what drugs are osmotic diuretics?
how do osmotic diuretics work?
-work at the proximal convoluted tubule and loop of Henle
-increased plasma osmolarity
*does not alter GFR
describe osmotic diuretics
-large molecular weight molecule (pulls water with it)
-filtered but is too large to reabsorb (filters fast!)
-acute expansion of intravascular fluid vol.
-use in craniotomies to reduce brain bulk
-decrease in CSF production
what are side effects of osmotic diuretics?
-increased intravascular fld. vol. until filtered
-rebound HTN in non-intact BBB (pulled in brain causing HTN in brain and increased ICP, resulting in rebound HTN)
-can exacerbate CHF
-electrolyte disturbance (not often)
describe mannitol use
-reduction of intracranial pressure and brain mass
-reduction of high intraocular pressure when unable to lower pressure by any other mechanism
-urinary excretion of toxic materials
*may need something to keep BP up
describe the aldosterone antagonist?
-competes with aldosterone
-allows secretion of Na+ and Cl-
-used in combination with thiazide diuretics, to hold on to K+
what are uses for spironolactone?
used for edema r/t
*both lead to increased aldosterone
*side effect may be hyperkalemia
describe potassium sparing diuretics
-spares potassium independent of aldosterone
-weak diuretic effects
-distal tubules and collecting ducts
-increased excretion of Na+, Cl-, and bicarb
*not used alone as an anti-HTN or for edema
*used in combination with loop diuretics to limit potassium losses in the distal tubule
what are side effects of potassium sparing diuretics?
*use catiously w/ pts. at risk for hyperkalemia, pts. using ACE inhibitors and NSAIDS (both cause increased K+)
describe carbonic anhydrase inhibitors (CAI)
-acetazolamide (Diamox), methazolamide (Neptazane)
-works in proximal tubules
-inhibiting CA blocks NaBicarb and causes diuresis
-used in glaucoma to reduce intraocular pressure by decreasing aqueous humor
what are side effects of CAIs?
-hyperchloremic metabolic acidosis