Diuretics. A. Kidney functions Kidneys have a number of essential functions:
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Transcript of Diuretics. A. Kidney functions Kidneys have a number of essential functions:
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Diuretics
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A. Kidney functions
• Kidneys have a number of essential functions:
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• 1. excretion
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• 2. regulate: • fluid balance • electrolyte composition • acid-base balance
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• 3. secrete enzyme renin
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• 4. secrete erythropoietin (a hormone that stimulates RBC production)
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• 5. produce calcitriol, the active form of vitamin D, which helps maintain bone homeostasis
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B. Kidney structure
• Each kidney contains more than 2 million nephrons, the functional unit of the kidney.
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• Each nephron is composed of several parts:
• glomerulus• proximal convoluted tubule (PCT)• loop of Henle• distal convoluted tubule (DCT)• collecting ducts
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• The glomerulus is the site where filtration of substances in the blood occurs.
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• Small molecules, electrolytes and water are filtered from the blood into the glomerular filtrate by passing through filtration slits and pores.
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• Molecules small enough to be filtered include:
• amino acids• creatinine• certain drugs• electrolytes• glucose• urea, uric acid• certain vitamins
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• They generally have a diameter < 8 nm.
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• Substances in the blood greater than 8 nm are retained in the blood, and include:
• blood cells• plasma proteins (i.e. albumin)• hormones
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• The rest of the nephron (PCT, loop of Henle and DCT) is involved with either:
• reabsorbing many of these small molecules, electrolytes, and water and transporting them back into the blood
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• Water is the most important molecule re-absorbed.
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• For every 180 liters (47 gallons) of water entering the filtrate each day, 178.5 liters are reabsorbed, leaving only 1.5 liters to be excreted in the urine.
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• or, secreting other waste products from the blood to the filtrate for removal in urine
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• After leaving the glomerulus the filtrate enters the PCT.
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• The PCT is the site where water, electrolytes (Na1+, Cl1-, and HCO3
1- ), glucose and amino acids are reabsorbed.
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• After leaving the PCT, the filtrate travels through the loop of Henle. This is the site of tubular reabsorption of water, Na1+, K1+, Ca2+, Mg2+, Cl1-, and HCO3
1- .
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• Next, the filtrate passes through the DCT. This is the site of tubular reabsorption of most ions including Na1+, K1+, Ca2+, Mg2+, Cl1-, and HCO3
1-.
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• The convoluted part of the distal tubule is virtually impermeable to water and urea.
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• The late distal tubule has a varying permeability to water, depending on the concentration of ADH.
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• When ADH is elevated, water is reabsorbed.
• In the absence of ADH, water is not reabsorbed.
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• Then the filtrate passes into tubes called collecting ducts where water may be reabsorbed, again dependent on ADH levels.
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• Diuretics are drugs that increase urine output.
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• This is considered a desirable effect in the treatment of the following conditions:
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• hypertension (HT)• heart failure (HF)• kidney failure • pulmonary edema • liver failure or cirrhosis
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• The most common way in which diuretics act is by blocking sodium reabsorption in the nephron, thus sending more of this ion into the urine.
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• Chloride ion also follows sodium
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• Water molecules also stay with both of these ions
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• Therefore, blocking the reabsorption of sodium will keep more water in the filtrate.
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• The more water retained in the filtrate, the greater the volume of urination, or diuresis.
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C. Categories of diuretics
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1. Thiazide diuretics
• Thiazide diuretics are some of the most widely used of the diuretic drugs.
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• The site of diuretic action for the thiazide diuretics is the early DCT.
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• Thiazides are the preferred diuretic in the treatment of HT, mild HF, and certain renal disease (nephrolithiasis, nephrogenic diabetes insipidus).
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• They cause a greater diuresis than the K1+ sparing diuretics, but a lesser diuresis than the organic acid diuretics.
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• They are the only diuretics which decrease Ca2+ excretion.
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• This results in a mild increase in serum Ca2+ levels, which decreases bone resorption (release of Ca2+ from bone).
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• They would be recommended for patients at risk of osteoporosis.
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• The distal tubule is the main site in the nephron for the secretion of K1+ , normally in exchange for Na1+ .
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• Thiazide diuretics work by inhibiting sodium reabsorption which increases its excretion, along with Cl1- and substantial amounts of water.
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• Thiazides do not interfere with K1+ .
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• Thiazide diuretics include:• chlorothiazide (diuril): 500 mg – 2,000
mg/day for both HT, edema.• Duration: 6 – 12 hours
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• hydrochlorothiazide (HydroDIURIL, Hydropar, Ezide):
• 25 - 50 mg/day for HT• 25 - 100 mg/day for edema• Duration: 6 – 12 hours
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• This drug is a derivative of chlorothiazide that is more popular than the parent drug.
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• It is more potent than chlorothiazide, so the required dose is considerably less.
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• methyclothiazide (Enduron, Aquatensen)• 2.5 – 5.0 mg/day for HT• 2.5 – 10.0 mg/day for edema• Duration: 24 hours
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• The thiazide-like diuretics are not the same chemically as the thiazides, but have the same effects.
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• Many have a longer duration of action than the thiazides.
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• chlorthalidone (Hygroton, Thalitone):• 15 - 50 mg/day for HT• 30 - 120 mg/day for edema• Duration: 24 – 72 hours
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• indapamide (Lozol)• 1.25 – 5.0 mg/day for HT• 2.5 – 5.0 mg/day for edema• Duration: up to 36 hours
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• metolazone (Zaroxolyn)• 2.5 – 5.0 mg/day for HT• 5.0 – 20 mg/day for edema• Duration: 12 - 24 hours• (Often used with an organic acid (loop)
diuretic in refractory HF due to systolic dysfunction).
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• Adverse effects commonly associated with the thiazide diuretics include:
• hypokalemia• hyponatremia in some elderly • hypochloremia • orthostatic hypotension
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• hyperglycemia• Hyperglycemia occurs primarily through
the reduction in total body potassium and the subsequent decreased insulin secretion.
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• hyperuricemia• Hyperuricemia is associated with the
condition gout (crystals of urate/uric acid depositing in tissues of the body).
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• Chronic gout can lead to deposits of hard lumps of uric acid in and around the joints, decreased kidney function, and kidney stones.
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• Thiazide diuretics decrease urate excretion by increasing net urate reabsorption. The mechanism by which this occurs is unclear.
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2. Organic acid diuretics
• This class is classified as organic acid diuretics because most of them contain a carboxylic acid functional group.
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• They are more commonly referred to as loop diuretics, as their site of action is the loop of Henle.
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• Organic acid diuretics are indicated for the treatment of edema (pulmonary, peripheral, and edema associated with ascites), HT, and acute renal failure.
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• These conditions require a greater diuretic action than is achieved with a thiazide diuretic.
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• They are often used in patients who have developed a resistance to the thiazides.
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• They promote diuresis by inhibiting Na1+ reabsorption in the loop of Henle.
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• This results in a greatly increased excretion of Na1+ ,Cl1-, and water.
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• They have the greatest Na1+ excretion, as well as the greatest Ca2+ excretion (not a desirable effect) of the diuretics.
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• The organic acid diuretics also result in an increase in K1+ secretion (they are equivalent to the thiazide diuretics in terms of this).
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• Organic acid diuretics include:• bumetanide (Bumex)• 0.5 – 10 mg/day• Duration: 4 – 6 hours
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• furosemide (Lasix) • 20-80 mg/day initially, may increase by 20-
40 mg• Duration: 4 – 6 hours
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• torsemide (Demadex)• 10-20 mg/day• 5 – 10 mg/day for edema associated with
cirrhosis (i.e. ascites)• Duration: 6 – 8 hours
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• The dose may be doubled until desired effect is observed (up to 200 mg, generally in the context of renal failure).
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• ethacrynic acid (Edecrin)• 50 – 200 mg/day• Duration: 6 – 8 hours
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• Adverse effects of the organic acid diuretics:
• Many of these are similar to the thiazides• hypokalemia• hyperuricemia• hyperglycemia • orthostatic hypotension
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• In addition:• They produce tone deafness in some
patients, especially if given in conjunction with an aminoglycoside antibiotic
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3. Potassium sparing diuretics
• This type of diuretic is used when there is a need to maintain normal levels of potassium in the patient along with the diuresis (i.e after MI).
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• Their site of action is the DCT, but farther along the tubule (closer to the collecting ducts) than the thiazides.
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• They prevent K1+ secretion in the distal tubules by altering the membrane or blocking aldosterone receptors, so that K1+ is not secreted in exchange for Na1+
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• Na1+ remains in the tubule.
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• When Na1+ reabsorption is blocked, the body retains more K1+.
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• Since most of the sodium has already been removed by the time the filtrate reaches the distal tubule, potassium sparing diuretics produce only a mild diuresis.
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• Their primary use is in combination with thiazide or organic acid diuretics to minimize potassium loss.
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• In patients with hepatic cirrhosis, potassium sparing diuretics are recommended along with either a loop or thiazide diuretic.
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• Potassium sparing diuretics are used alone when the patient has an excess of aldosterone (secondary hyperaldosteronism)
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• Potassium sparing diuretics include:• amiloride (Midamor)• 5-10 mg/day• Duration: up to 24 hours
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• spironolactone (Aldactone) • 50 – 100 mg/day for treatment of edema,
HT• 100 – 400 mg/day for treatment of
hyperaldosteronism• Duration: 48 – 72 hours
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• eplerenone (Inspra)• 25 – 50 mg/day• Duration: 12 – 24 hours
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• triamterene (Dyrenium)• 100 – 200 mg/day• Duration: 12 – 16 hours
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• Combination diuretics• spironolactone with hydrochlorothiazide
(Aldactazide)• triamterene with hydrochlorothiazide
(Dyazide, Maxzide)
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• These combination diuretics are recommended in patients with diabetes or impaired renal function to prevent hyperkalemia
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• Adverse effects of the potassium sparing diuretics:
• hyperkalemia • nausea, diarrhea