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Flashcards in diuretics Deck (30)
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1
Q

what are forces that favor filtration?

A
  • glomerular hydrostatic pressure 60 mmHg (pushing out)

- bowman’s capsule colloid osmotic pressure of 0 (pulling in)

2
Q

what are forces that oppose filtration?

A

bowman’s capsule hydrostatic pressure 18 mmHg (pushing against)
glomerular capillary osmotic pressure 32 mmHg (pulling in)

3
Q

what is the net filtration pressure in the glomerular capsule?

A

10 mmHg

4
Q

what is the best way to increase urine output?

A

increase perfusion to kidneys by increasing BP, which increases filtration pressure

5
Q

how is GFR normally preserved?

A

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

6
Q

describe autoregulation

A
  • 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
7
Q

what makes up urine besides water?

A

solutes

  • electrolytes: primarily sodium, potassium, chloride, and bicarbinates
  • waste products: creatinine
  • pharmacologic metabolites
8
Q

what determines urine excretion rate?

A

filtration rate - reabsorption rate + secretion rate

9
Q

what are uses for diuretics?

A
  • 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
  • drug clearance
10
Q

which drugs are loop diuretics?

A
  • furosemide (Lasix)
  • torsemide (Demadex)
  • bumetanide (Bumex)
  • ethacrynic Acid (Edecrin)
11
Q

what is the MOA of loop diuretics?

A

inhibit reabsorption of NaCl in ascending loop of Henle

  • stimulate production of prostaglandins (vasodilation, increased RBF)
  • non increase in GFR
12
Q

describe loop diuretics

A
  • 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.)
13
Q

what are some clinical uses of loop diuretics?

A
  • rapid intravascular fld. removal
  • hyperkalemia
  • acute pulmonary edema
  • kidney stone extraction, lithotripsy
  • reduce intracranial pressure (systemic diuresis and decreased CSF production; used w/ mannitol)
14
Q

what are concerns with loop diuretics?

A
  • 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)
  • mild hyperglycemia
15
Q

what drugs are thiazide diuretics?

A
  • chlorothiazide (Diuril)
  • chlorthalidone
  • indapamide (Lozol)
  • hydrochlorothiazide (Microzide, Esidrix)
  • benzthiazide
  • cyclothiazide
  • metolazone (Zaroxolyn)
16
Q

what is the MOA of thiazide diuretics?

A
  • 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+
17
Q

what are clinical uses of thiazide diuretics?

A
  • reduces edema (edema from CHF)
  • reduces intravascular fld. vol (HTN)
  • renal failure
  • used in combination with antihypertensive drugs
18
Q

what are effects of thiazide diuretics?

A
  • decreased K+, Mag++, Cl-
  • hypochloremic metabolic alkalosis
  • hyperglycemia
  • 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)
19
Q

what drugs are osmotic diuretics?

A
  • mannitol

- urea

20
Q

how do osmotic diuretics work?

A
  • work at the proximal convoluted tubule and loop of Henle
  • osmotic diuresis
  • increased plasma osmolarity
  • does not alter GFR
21
Q

describe osmotic diuretics

A
  • 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
22
Q

what are side effects of osmotic diuretics?

A
  • 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)
  • pulmonary edema
  • can exacerbate CHF
  • electrolyte disturbance (not often)
  • give slow
23
Q

describe mannitol use

A
  • 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
24
Q

describe the aldosterone antagonist?

A
  • spironolactone (Aldactone)
  • competes with aldosterone
  • allows secretion of Na+ and Cl-
  • used in combination with thiazide diuretics, to hold on to K+
25
Q

what are uses for spironolactone?

A

used for edema r/t

  • CHF
  • Liver Cirrhosis
  • both lead to increased aldosterone
  • side effect may be hyperkalemia
26
Q

describe potassium sparing diuretics

A
  • triamterene, amiloride
  • 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
27
Q

what are side effects of potassium sparing diuretics?

A

primarily hyperkalemia

*use catiously w/ pts. at risk for hyperkalemia, pts. using ACE inhibitors and NSAIDS (both cause increased K+)

28
Q

describe carbonic anhydrase inhibitors (CAI)

A
  • 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
29
Q

what are side effects of CAIs?

A
  • hyperchloremic metabolic acidosis
  • drowsiness
  • paresthesia
  • renal calculi
30
Q

what are some combination drugs with diuretics?

A
  • spironolactone/HCTZ (Aldactazide)
  • triamterene/HCTZ (Dyazide)
  • Hydralazine/HCTZ (Hydra-Zide)
  • Clonidine/Chlothalidone (Clorpress)