Unit 3 Study Guide
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, Study Guide Pharmacology Exam Unit 3
CH 35 Diuretics
How diuretics work:343-344
Blockade of sodium and chloride reabsorption. By blocking the reabsorption of these solutes,
diuretics create osmotic pressure within the nephron that prevents the passive reabsorption of
water and increase urine production.
Diuretics causes water and solutes to be retained within the nephron and promote the
excretion of both.
Increase urine flow directly related to the amount of sodium and chloride reabsorption that it
blocks.
Drugs that block solute reabsorption to the greatest degree, produces the most profound
diuresis.
Because the amount of solutes in the nephron becomes smaller as filtrates flows from the
proximal tubules to the collecting ducts, drugs that act early in the nephron have the
opportunity to block the greatest amount of solutes reabsorption. Theses drugs produces the
greatest diuresis.
Diuretics increase urine output to 1.8/L for each 1% of solute reabsorbed/blocked.
3% blockade of solute reabsorption will produce 5.4/L of urine a day-fluid loss, reduces body wt
by 12 lbs in 24 hours. Normal urine production is 180/L per day
Adverse effects: (can be minimized by using short-acting diuretics and by timing administration such
that the kidney is allowed time to operate in a drug free manner between periods of diuresis).
Hypovolemia (from excessive fluid loss)
Acid-base imbalance
Altered electrolyte levels.
Classification of diuretics:
1. Loop diuretics (furosemide)
2. Thiazide diuretics (hydrochlorothiazide)
3. Osmotic diuretics (mannitol)-reduces IOP
4. Potassium sparing agent- 2 types: aldosterone antagonists-(spironolactone) and non-
aldosterone antagonists-(triamterene).
5. Carbonic anhydrase inhibitors -primarily to lower intraocular pressure (IOP) not to increase
urine production.
, Loop Diuretics pg 344
Furosemide (Lasix) pg 344 Adverse effects Drug interactions
Indicated for: (1) pulmonary edema associated Excessive loss of sodium, chloride and water. Digoxin-increases risk for
with congestive heart failure. Magnesium deficiency (muscle weakness, tremor, dysrhythmias. Low potassium
(2) edema of hepatic, cardiac or renal origin that twitching, dysrhythmias) and Hypercalcemia increase risk for digoxin induced
has been unresponsive to less efficacious results toxicity (ventricular dysthymias). K+
diuretics (3) hypertension that cannot be Severe dehydration (dry mouth, unusual thirst, should be monitored. Potassium
controlled with other diuretics. oliguria). Excessive wt loss. If dehydration occurs. supplement or a potassium sparing
diuretic should be used.
Furosemide should be withheld. Can minimize by
Use in pts with severe renal -can promote
starting with low doses. Daily wts.
diuresis even when renal blood flow and Ototoxic drugs- risk for furosemide
glomerular filtration rates (urine) are low. Hypotension (loss of volume and relaxation of induced hearing loss. Especially in
venous smooth muscle, which reduces combination with aminoglycoside
Thiazides may be added but do not added with venous return to the heart) s/s-dizziness, antibiotics (gentamicin). Drugs
another loop diuretic (no benefit). lightheadedness, fainting. should be avoided.
Hypokalemia-potassium is loss through increased
Acts in the thick segment of the ascending limb secretion in the distal nephron. If serum k+ falls Potassium sparing diuretics-
of the loop of Henle to block reabsorption of below 3.5 meq, fatal dysrhythmias may result. spironolactone, triamterene can help
sodium and chloride. By blocking solutes (Foods high in K+ dried, fruits, nuts, spinach, balance the potassium wasting
reabsorption, furosemide prevents passive potatoes, bananas). Add k+ supplement or use a effects of furosemide and reduce risk
reabsorption of water. potassium -sparing diuretic of hypokalemia.
Ototoxicity-hearing impairment. Deafness is
Dosing – Lithium-pts with low sodium,
transient. Ability to impair hearing. Use in caution
20, 40, 80 mg tablets excretion of lithium is reduced, by
with other otoxic drugs (aminoglycoside
Onset 60 mins lowering sodium, lithium will
Duration 6-8 hours antibiotics. accumulate to toxic levels. Lithium
Dose 20-80 mg; 1-2 per day Hyperglycemia-elevation of plasma glucose is a levels should be monitored, and if
potential. Appears from inhibition of insulin too high, lithium dose should be
Oral administration, diuresis begins in release. When a diabetic takes furosemide the pt reduced.
60 minutes and persist for 8 hours. Oral is used should monitor blood glucose level.
when rapid onset is not required. Hyperuricemia-elevation of plasma uric acid. Antihypertensive agents-may need to
Induced hyperuricemia is asymptomatic. Pts with reduce or eliminate use of other
Undergoes hepatic metabolism followed by gout, elevation of uric acid may precipitate a gouty hypotensive medications to prevent
renal excretion. attack (tenderness or swelling joints) hypotension.
Reduces high density lipoprotein (HDL) cholesterol
Nonsteroidal anti-inflammatory
and raises low density lipoprotein (LDL) cholesterol
Monitor: drugs-aspirin and other NSAIDS can
and triglycerides. Reduces risk for coronary heart
b/p reduce the effects for furosemide
disease.
daily wts effect. Inhibition of prostaglandin
cbg in DM Can cause profound diuresis with water and synthesis in the kidney, increasing
k+ electrolyte depletion. renal blood flow, which occurs
electrolytes Pregnancy through prostaglandin mediated
uric acid Caused maternal death, abortion, fetal process.
hearing resorption in animals.
Used only if absolutely required.
, Ethacrynic acid (Edecrin) Torsemide (Demadex) Bumetanide (Burinex) generic only in US
Used for: edema caused by heart failure, Used for: edema caused by heart failure, Used for: edema caused by heart failure, chronic
chronic renal disease and cirrhosis chronic renal disease and cirrhosis renal disease and cirrhosis
Approved for hypertension
Dosing- Dosing-
50-100 mg/ 1-2 per day Dosing- 0.5-2 mg; 1 per day
Onset within 30 minutes 5-20 mg; 1 per day Onset 30-60 minutes
Duration – 6-8 hours Onset-within 60 min Duration 4-6
Duration – 6-8 hours
Promote diuresis by inhibiting sodium and Promote diuresis by inhibiting sodium and
chloride reabsorption in the thick Promote diuresis by inhibiting sodium chloride reabsorption in the thick ascending limb
ascending limb of the loop of henle. and chloride reabsorption in the thick of the loop of henle
ascending limb of the loop of henle
Side effects- ototoxicity, hypovolemia, Side effects- ototoxicity, hypovolemia,
hypotension, hypokalemia, hyperuricemia, Side effects- ototoxicity, hypovolemia, hypotension, hypokalemia, hyperuricemia,
hyperglycemia, and disruption of lipids hypotension, hypokalemia, hyperglycemia, and disruption of lipids
metabolism hyperuricemia, hyperglycemia, and metabolism
disruption of lipids metabolism
Drug interactions-NSAIDS decreases drug Drug interactions-NSAIDS decreases drug effects,
effects, ototoxicity caused by Drug interactions-NSAIDS decreases drug ototoxicity caused by aminoglycosides, digoxin
aminoglycosides, digoxin increases effects, ototoxicity caused by increases cardiotoxicity risk and causes lithium
cardiotoxicity risk and causes lithium aminoglycosides, digoxin increases levels to accumulate leading to lithium toxicity
levels to accumulate leading to lithium cardiotoxicity risk and causes lithium
toxicity levels to accumulate leading to lithium
toxicity
Osmotic diuretic
Mannitol
Osmotic diuretic-occurs naturally in sugar and alcohol. Causes the body to lose water through osmosis.
Promotes diuresis in the kidneys by increasing the concentration of filtrates in the kidney and blocking
reabsorption of water by the kidney tubules. Elevates blood plasma osmolality, enhances flow of water from
tissues including brain and cerebrospinal fluid volume.
Used to reduce intracranial pressure associated with cerebral edema or brain mass, kidney failure, glaucoma,
increase in bodi
12.5 g/kg IV infused over 30-60 minutes, repeat every 6-8 hours