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DIURETICS· Amongthe most commonly used drugs.· Increasesodium and water excretion by the kidney through inhibition of renal sodiumtransport.· 1ouses: treat edema and hypertension.· “Waterpills” FUNCTIONS OF THE KIDNEY· Fluidvolume and solute homeostasis.o Watero Electrolytes(Na+, K+,...  
DIURETICS· Amongthe most commonly used drugs.· Increasesodium and water excretion by the kidney through inhibition of renal sodiumtransport.· 1ouses: treat edema and hypertension.· “Waterpills” FUNCTIONS OF THE KIDNEY· Fluidvolume and solute homeostasis.o Watero Electrolytes(Na+, K+, Cl-, Ca++, Mg++, phosphate, sulfate)o Acid-basebalance· Excretionof metabolic wastes, drugs and other foreign compounds.· Endocrine:production of erythropoietin, active Vitamin D, vasoactive mediators (renin).· Regulationof blood pressure RENAL ANATOMY Urine is formed byfiltration in the glomerulus, modified by the nephron, and then drains  calyces  renalpelvis  ureter   bladder  urethra. HUMAN KIDNEYEach kidney weighs ~150 g.Size: 11 cm long x 6 cm wide x 3 cm thick(size of deodorant stick).Only need 1 kidney for survival-remainingkidney compensates by increasing functional activities. The kidney can repairitself to some extent, but it does not form new nephrons. NEPHRONFunctional unit of the kidney· •~1million nephrons/kidney· •Twocomponents: v  VascularAfferentarteriol  Glomerularcapillaries  Efferentarteriole  Peritubularcapillaries-cortex  Vasa recta-medulla v  TubularProximal tubule(PCT)   Loop of Henle (LOH) (thin descending,thin ascending, thick ascendinglimbs)  Distal tubule(DCT)  Collecting Duct (CD) URINE FORMATION AND MODIFICATION · Theprocess of urine formation begins with filtration into theglomerulus. In the glomerular capillaries, the hydrostatic pressure of theblood forces ~20% of the plasma to filter into the nephron. · Thisultrafiltrate contains all the substances present in plasma, in the sameconcentration as in plasma, except for red blood cells and plasma proteins, andsubstances bound to these proteins, which are retained in the blood. · Afterplasma is filtered and the ultrafiltrate enters the nephron, tubular transportprocesses alter the concentration of substances in the ultrafiltrate, whichdetermines how much is excreted · Tubulereabsorption removes solutes from filtrate and returns them toblood. · Tubulesecretion removes solutes from blood and adds them to thefiltrate.  GLOMERULAR FILTRATIONFirst step in urine formation.•Glomerulus acts as a sieve - permits waterand ions through, but not red blood cells or proteins (or drugs boundto proteins).•3 layers in sieve: capillary endothelium,basement membrane, podocytes.•Capillary hydrostatic pressure forces 20% ofthe plasma fluid to filter into the nephron.GFR = glomerular filtration rate 125 ml/min TUBULAR SECRETION· Servesas a supplemental elimination mechanism – allows more to be excreted than wasfiltered.· Mainmechanism for urinary excretion of many drugs.· Particularlyimportant for drugs that bind to plasma proteins and are not filtered intourine by glomerulus.· Importantfor excretion of H+ and K+· Transportfrom blood to urine TUBULAR REABSORPTION· Selectivemovement from urine back to blood.· Renalblood flow = 1.2 L/min -- entire blood volume circulates through the kidneys in4-5 min or 300 times a day!· Renalplasma flow = 55% x 1.2 L/min = 660 mL/min.· Since~19% of renal plasma flow is filtered by the glomerulus, 19% x 660 mL/min = 125mL/min, equal to 180liters ofultrafiltrate produced each day!· Virtuallyall filtered solutes and water are returned to the circulation by tubularreabsorption, and only small amounts are excreted. Water – 180 L filtered perday, 1.5 L excreted. A DAY IN THE LIFE OF YOUR KIDNEYS· Normalglomerular filtration rate (GFR) is 125 ml/min.· Withrenal disease, GFR decreases, so less fluid and solutes are filtered, resultingin decreased excretion of water and solutes.· GFRis typically calculated from measurements of serum creatinine levels; anincrease in serum creatinine means that GFR has decreased. PROXIMAL TUBULE · Reabsorbs:o Sodium(65% of filtered sodium).o Water,osmotically driven by sodium reabsorption (65% of filtered water).o Chloride,potassium, bicarbonate, calcium, magnesium, phosphate, sulfate.o Allfiltered organic solutes such as glucose and amino acids.· Secretes:o Protons(acidifies urine).o Organicacids and bases (drug excretion). LOOP OF HENLE Sodium & WaterReabsorption · ThinDescending limbo Passivelyreabsorbs water driven by osmotic gradient in medullary interstitial fluid.o LowNa+ permeability · ThinAscending Limbo Passivelyreabsorbs Na+ that was concentrated in urine by water reabsorption in thindescending limb.o Lowwater permeability. · ThickAscending Limb (Diluting Segment)o ReabsorbsNa+ on Na-K-2Cl cotransporter-contributes to medullary interstitial fluidosmolality in medullary portion.o Lowwater permeability.        SODIUM & WATER REABSORPTION· DistalConvoluted Tubuleo Reabsorbssodium on NaCl cotransporter· CollectingDucto Siteof final urine modificationo Reabsorbssodium (controlled by aldosterone)o Secretespotassiumo Secretesprotons (can reduce urine pH to 4.5-5)o Reabsorbswater relative to antidiuretic hormone (ADH or vasopressin), to form a concentrated(+ ADH) or dilute (no ADH) urine ANTIDIURETIC HORMONE· Inthe absence of antidiuretic hormone (ADH) the collecting duct is impermeable towater.· ADHcauses insertion of water channels (aquaporins) in the cell membrane ofcollecting duct cells.· Thesewater channels allow water to be reabsorbed, driven by the high osmolality ofthe medullary interstitial fluid.· ADHdeficiency results in a disease known as diabetes insipidus, characterized byexcretion of large volumes of dilute urine BODY FLUID COMPARTMENTS· Totalbody water = 60% body weight.· Intracellular(28liters) = fluid inside cells.· Extracellular(14liters) = fluid outside of cells.o Interstitialfluid (11liters) = fluid surrounding cellso Plasma(3 liters) = fluid component of blood· Edemais the accumulation of excess fluid in the interstitial compartment.· Clinicallyapparent with ~3 liter increase in interstitial fluid volume.· Renalsodium and water retention maintains and enhances edema (notgood).  REGULATION OF EXTRACELLULAR FLUID(ECF) VOLUME BY THE KIDNEY· BecauseNa+ is the major osmotically active ion in the ECF, total body Na+ contentdetermines ECF volume. The kidney regulates extracellular fluid volume byadjusting the amount of Na+ excreted.   VOLUME DEPLETION  Sympathetic nervesRenin-angiotensinAldosteroneAntidiuretic hormone  Decrease GFRIncrease Na+ reabsorption  Decreased Na+ excretionDecreased urineoutput VOLUMEOVERLOAD ProstaglandinsAtrial natriureticpeptide  Increase GFRDecreaseNa+reabsorption Increased Na+ excretionIncreased urineoutput    RENIN-ANGIOTENSIN-ALDOSTERONESYSTEM · Renin,released by the kidney, cleaves angiotensin I from angiotensinogen made byliver.· AngiotensinI is converted to angiotensin II by angiotensinconverting enzyme (ACE).· AngiotensinII stimulates aldosterone secretion from adrenal gland.· Aldosteroneand angiotensin II increase Na+ reabsorption, resulting in Na+ retention andincreased plasma volume.· Pharmacologicalagents such as ACE inhibitors and angiotensin II receptor blockers selectivelyblock the renin-angiotensin-aldosterone system and can be used to treat highblood pressure. EVENTS LEADING TO SYSTEMIC EDEMA · Thebody uses pressure to monitor fluid volume.· Adrop in pressure (e.g. hemorrhage) activates regulatory mechanisms such as thereninangiotensin-· Aldosteronesystem to conserve sodium and water.· Theseregulatory mechanisms are also activated with some diseases associated withpressure changes (heart, kidney, liver disease). The pressure drop “fools” thekidney into thinking that volume is low when it’s not, resulting in edema.· Themajor edematous states (CHF, liver cirrhosis) are characterized by persistentrenal Na+ retention despite progressive expansion of ECF volume.  DIURETICS· Among the most commonly used drugs.· 1o uses: to treat edematous states and hypertension.· Diuretics do not directly affect water transport. They actindirectly by inhibiting sodium reabsorption at various sitesalong thenephron, resulting in more water and sodium excretion.· Increased output of urine - “diuresis”.· Increased output of sodium - “natriuresis”.· 180L filtrate/day…almost all reabsorbed.·  Foreach 1% of solute reabsorption blocked, urine output increases by 1.8 L.· 3%blockade = 5.4 L urine/day = 12 lb. weight loss.· Smallblockade can have profound effects.    SOME CLINICAL USES OF DIURETICSPrimary Uses:•Edematousstates  •Hypertensiona.Congestive heart failureb.Hepatic cirrhosis with ascitesc. RenaldiseaseSecondary Uses of Select Diuretics:•Prevent renal failureby maintaining urineflow •Kidneystones•Acute treatment of hypercalcemia  •Glaucoma•Altitude sickness  •Diabetesinsipidus  > DIURETIC CLASSES     1.  Carbonic anhydrase inhibitors ·  acetazolamide 2.  Loop diuretics ·  furosemide 3.  Thiazide diuretics ·  hydrochlorothiazide 4.  Potassium-sparing diuretics: ·  Aldosterone antagonists ·  Sodium channel blockers   ·  Spironolactone ·  triamterene 5.  Osmotic diuretics       · #s 1-4 prevent passive water reabsorption by inhibiting sodiumreabsorption by the kidney       DIURETICS: MECHANISMS OF ACTION Diuretics may act by:•Inhibition of sodium transporters atdifferent parts of the nephron -- loop diuretics, thiazides, sodium channelblockers.•Osmotic effects to prevent waterreabsorption-- mannitol.•Enzyme inhibition -- acetazolamide.•Interaction with hormone receptors -- spironolactone.  DIURETICS:ADVERSE EFFECTS•Diuretics compromise normaloperation of the kidney to promote excretion of water.•Common side effects:–Hypovolemia(leads to hypotension)–Loss/gainof electrolytes–Acid-baseimbalance•Blocking sodium reabsorption atone nephron site can interfere with other renal functions linked to it.•Blocking sodium reabsorption atone nephron site can alter transport activity at other nephron sites.•Most adverse effects areapparent by 2 weeks.        DIURETIC EFFICACY v  Increasein urine flow produced by a diuretic is directly related to the amount of Na+reabsorption that the drug blocks.Depends on:•Amountof sodium reabsorbed atthe diuretic-sensitive site in thenephron.•Reabsorptionof sodium by moredistal nephron segments.•Luminalaccess (blocktransporters on luminal membrane).  v  Drugswhose site of action is early in the nephron have the opportunity to block thegreatest amount of solute reabsorption     DIURETIC EFFICACY Luminal Access• Exceptfor spironolactone, all diuretics act within the tubular lumen.• Little filtration due toprotein binding.• Gain luminal entry by tubularsecretion in the proximal tubule (except mannitol, which is just filtered). DIURETICS & Na+ REABSORPTION ALONG THENEPHRON      > Nephron Segment % Filtered Na+ Reabsorbed Diuretic Class   Target Proximal tubule   65% Carbonic anhydrase inhibitors   Carbonic anhydrase   Thick ascending limb 20% Loop diuretics   Na,K,Cl cotransporter   Distal tubule   10% Thiazide diuretics   NaCl cotransporter   Collecting duct   1-5% K+-sparing diuretics   Na channel     RELATIVEEFFICACY OF DIURETIC DRUGS align=left > Diuretic Agent Peak Urine Flow Rate (ml/min)  Control 1 Osmotic Diuretics 8 Carbon anhydrase inhibitors 12 Loop Diuretics 12 Thaizide Diuretics 5 K+ sparing diuretics 3                                    Drugs  >   PROXIMAL TUBULE: CARBONIC ANHYDRASE INHIBITORS Mechanism of  Action ·  Inhibits the enzyme carbonic anhydrase in the proximal tubule. ·  Indirectly blocks Na+ reabsorption by the Na/H exchanger (1) by reducing supply of protons. ·  Inhibition of Na+ reabsorption blocks passive water reabsorption. ·  Increased urinary excretion of sodium, bicarbonate, potassium, and water, and increased urine pH (more alkaline).   Therapeutic Uses Generally given for reasons other than diuresis. ·  Treatment of metabolic alkalosis, particularly with fluid load. ·  Induce urinary alkalinization. ·  Glaucoma – most common indication; dorzolamide, brinzolamide – topical CAIs; reduce intraocular pressure. ·  Acute mountain sickness (altitude sickness).   v  Inhibit cerebral spinal secretion   Pharmacokinetics Near complete oral absorption. • Diuresis within 30 minutes, maximal at 2 hours, persists for 12 hours after a single dose. • Plasma half-life ~10 h. • Renal route of excretion.   Adverse Effects •Metabolic acidosis due to urinary loss of bicarbonate (limits use to 2-3 days). •Kidney stones (Ca2+ salts insoluble in alkaline urine)   v  Urine becomes very alkaline •Hypokalemia.  •Sulfonamide hypersensitivity.      LOOP(HIGH-CEILING) DIURETICS   Mostefficacious diuretics Sulfonamide derivatives•Furosemide (Lasix®)-most frequentlyprescribed  •Torsemide (Demadex®) •Bumetanide (Bumex®) Phenoxyacetic acid derivative•Ethacrynic Acid (Edecrin®) align=left >   LOOP (HIGH-CEILING) DIURETICS   Mechanism of   Action ·  All loop diuretics inhibit sodiumreabsorption by blocking the Na,K,Cl cotransporter in the ·  thick ascending limb of the loop of Henle (normally reabsorbs 20% filtered sodium). ·  Inhibition of Na+ reabsorption blocks passive water reabsorption, resulting in increased excretion of sodium ·  and water. ·  Inhibition of the Na,K,Cl cotransporter indirectly prevents reabsorption of calcium and magnesium.   Therapeutic Uses Particularly useful since loop diuretics can promote dieresis when GFR is low. Used for: ·  Rapid fluid mobilization o  Pulmonary edema due to CHF ·  Treat edema (hepatic, cardiac, or renal disease) particularly when unresponsive to other diuretics ·  Hypertension uncontrolled by other diuretics o  Particularly with renal disease ·  Acute hypercalcemia ·  Anion overdose o  Inhibits reabsorption of Br-, F   Pharmacokinetics Can be administered po, iv, im. ·  Oral, diuresis in 30-60 min, 6-8 hour duration. ·  IV furosemide (rapid treatment of pulmonary edema), diuresis in 5 min, 2 hour duration. ·  Eliminated by renal secretion and filtration. ·  t1/2 (1-4 hour), dependent on renal function.   Adverse Effects •Hypovolemia •Hypotension: due to volume depletion and vasodilatation(hypotension sign, include: dizziness,lightheadness,fainting) •Electrolyte imbalance - increased excretion leading to: -Hyponatremia -Hypochloremia -Hypokalemia (fatal may result in dysrhythmias) -Hypocalcemia -Hypomagnesemia   v  signs dry mouth, unusual thirst, and oliguria (excessive weight loss) •Metabolic alkalosis •Hyperuricemia (gout: due to elevation of uric acid) •Metabolic: hyperglycemia(due o inhibition of insulin release), hyperlipidemia (can increase risk for coronary disease) •Sulfonamide hypersensitivity (except ethacrynic acid) •Ototoxicity( deafness is transient)   Drug Interaction Ototoxicity (caution aminoglycosides)   v  The risk of induces hearing loss is increased w/ concurrent use of other ototoxic drugs especially aminoglycosides Digoxin toxicity – hypokalemia   v  In the presence of low k+ levels the risk of serious digoxin induced toxicity is greatly increase (dysrhytmias) Lithium toxicity due to decreased excretion (in the presence of low sodium levels, excretion of lithium is decrease) NSAIDS blunt diuretic effect -Inhibits prostaglandins synthesis, NSAIDS prevent the increase in renal blood flow and blunt diuretic effects    THIAZIDE DIURETICS•All have unsubstitutedsulfonamide group.•Similar effects as loopdiuretics…less efficacy.– Hydrochlorothiazide (HydroDIURIL®)– Indapamide (Lozol®)– Chlorthalidone (Hygroton®)– Chlorothiazide (DIURIL®)– Quinethazone (Hydromox®)– Metolazone (Zaroxolyn®, Mykrox®)  width=881 >   THIAZIDE DIURETICS: DISTAL TUBULE   Mechanism of  Action •Most commonly prescribed class of diuretics. •Inhibit the NaCl cotransporter in the distal convoluted tubule. •Milder diuresis compared to loop diuretics because this nephron site reabsorbs less sodium (10% of filtered load). •Less effective than loop diuretics in patients with renal insufficiency (in patients with low GFR, most of the fluid is reabsorbed by the time it reaches the distal convoluted tubule).   v  The ability of ability of thiazide to promote dieresis is dependent on adequate kidney function Thiazides inhibit sodium reabsorption by blocking the NaCl cotransporter in the distal convoluted tubule. •Inhibition of Na+ reabsorption blocks passive water reabsorption, resulting in increased excretion of sodium and water.     Therapeutic Uses ·  Hypertension -- 1st line therapy for mild-to-moderate HTN; effective, safe and cheap ·  Edema due to mild heart, kidney or liver disease ·  In combination with loop diuretics, for severe, resistant edema ·  Idiopathic hypercalciuria ·  Diabetes insipidus (decrease urine production by 30%-50%) ·  THIAZIDE USE IN HYPERCALCIURIA •Recurrent kidney stone formation due to excessive calcium excretion. •Thiazides increase distal tubular Ca2+ reabsorption. •Prevent “excess” excretion which could form stones.       Pharmacokinetics •Rapid GI absorption. •Onset of action 1-2 hr; effects can be long lasting (typically 6-12 hr), but vary with the drug used.     Adverse Effects Similar to loop diuretics except no ototoxicity or hypocalcemia • Hypovolemia, hypotension (particularly in the elderly) • Electrolyte imbalance - increased excretion leading to: – Hyponatremia – Hypochloremia – Hypomagnesemia – Hypokalemia • Metabolic alkalosis • Hyperuricemia (gout) • Metabolic: hyperlipidemia, hyperglycemia • Sulfonamide hypersensitivity   Drug Interaction • Digoxin toxicity – hypokalemia. • Lithium toxicity – decreased excretion. • NSAIDS decrease diuretic effect. • Unlike loop diuretics, no ototoxicity.      MECHANISM OF DIURETIC INDUCED HYPOKALEMIA ANDMETABOLIC ALKALOSIS•Inhibition of Na+ reabsorption by loop orthiazide diuretics increases the amount of Na+ delivered to the collectingduct.•This results in increased Na+ reabsorptionby the collecting duct, which drives K+ and proton secretion.•Increased excretion of K+ and H+ leads tohypokalemia and metabolic alkalosis.•Particularly pronounced with highaldosterone levels (due to more Na+ channels). TREATMENT OF HYPOKALEMIA DUE TO LOOP ORTHIAZIDE DIURETICS• Reduce dietary NaClintake ( decrease collectingduct Na+ reabsorption  decreaseK+ secretion).• Increase dietary K+ intake (bananas, orangejuice).• K+ supplements.• Add K+-sparing diuretics. POTASSIUM-SPARING DIURETICS: COLLECTING DUCT •Cause mild increase in Na+ excretion &urine output.•Unlike thiazide & loop diuretics whichincrease K+ excretion, these diuretics decrease K+ excretion.• 2 types:1.  Aldosteronereceptor antagonista. Spironolactone2.  Sodiumchannel blockersa. Triamterineb. Amiloride POTASSIUM-SPARING DIURETICS: MECHANISM OFACTION•Relatively weak diuretics due to lowcapacity for Na+ reabsorption in collecting duct. Least efficacious.•Amiloride and triamterine directly inhibitNa+ reabsorption in collecting duct by blocking Na+ channels.•Spironolactone does not directly inhibit Na+channels, but prevents Na+ channel synthesis induced by aldosterone        >   K-SPARING DIURETICS: Na+ CHANNEL BLOCKERS   Mechanism of  Action ·  Amiloride and triamterine directly inhibit Na+ reabsorption in collecting duct by blocking Na+ channels. ·  Direct inhibitor of the exchange mechanism itself decrease Na+ uptake and a reduction of K+ secretion   Therapeutic Uses Used in combination with loop or thiazide diuretics to: • Augment their diuretic and antihypertensive effects. • Counteract the K+-wasting effects of thiazide and loop agents to prevent hypokalemia.   v  Used with as a combination with other diuretics to treat hypertension and edema   Pharmacokinetics Triamterine (Dyrenium®) –50% absorption of oral dose –Extensive hepatic metabolism with active metabolites –Onset of action: 2-4 hr; duration: 12-16 hr Amiloride (Midamor®) –50% absorption of oral dose –Not metabolized, excreted in urine unchanged –Onset of action: 2 hr; duration: 24 hr   Adverse Effects & Drug Interactions • Hyperkalemia (amiloride and triamterine) –Due to decreased potassium excretion –Avoid K+ supplements –Do not use in combination with spironolactone –Caution with ACE inhibitors • Kidney stones (triamterine)             >   K-SPARING DIURETICS: SPIRONOLACTONE (Aldactone®)   Mechanism of  Action •Receptor antagonist of aldosterone. •Aldosterone increases synthesis of Na+ channels in collecting duct. •Spironolactone competes with aldosterone for binding to mineralocorticoid receptors, which prevents production of Na+ channels.   Therapeutic Uses •Used in combination therapy with loop or thiazide diuretics to increase diuresis and/or prevent hypokalemia. •Particularly useful in primary aldosteronism (adrenal adenomas) and secondary aldosteronism (CHF, cirrhosis, kidney disease)   Pharmacokinetics •Slow onset of action -- need to get rid of sodium channelsalready formed …1-2 days.   v  Aldosterone acts by stimulating cells of the distal nephron to synthesize the proteins required for Na+ snf k+ transport. By preventing aldosterone action spironolactone blocks the synthesis of new proteins but does not stop exsting transport proteins from doing their job •Active metabolite canrenone formed in liver; has t1/2 = 16 h. •Duration of effect: 48-72 hours.   Adverse Effects & Drug Interactions •Hyperkalemia •Avoid K+ supplements •Do not use in combination with triamterine or amiloride •Caution with ACE inhibitors •Endocrine effects: gynecomastia, impotence, menstrual irregularities, hirsutism         OSMOTIC DIURETICS  v Osmotic diuretics differ from other diuretics both in mechanism ofaction and indications for use >   Mannitol (Osmitrol®)   Mechanism of  Action • A sugar that is freely filtered, not reabsorbed or metabolized, and pharmacologically inert. • Creates osmotic force within lumen of nephron – prevents H2O reabsorption in segments freely permeable to H2O (proximal tubule and thin descending limb). • Degree of diuresis related to amount of mannitol in filtrate. • Does not produce diuretic effects by blocking reabsorption of Na+.   Therapeutic Uses • Prophylaxis of renal failure under certain conditions increases urine flow to help prevent kidney shutdown when GFR is very low. • Reduction of intracranial pressure due to cerebral edema: draws fluid out of brain. Primary use   Pharmacokinetics • IV use only, not absorbed by GI tract. • Diuresis begins within 30-60 minutes and persists 6-8 hours.   Adverse Effects & Drug Interactions • Edema - use with caution in patients with heart disease.    DIURETICS: THERAPEUTIC CONSIDERATIONS•To minimize adverse effects, time doses to allow drug-freeperiods between periods of diuresis -- allows kidneys to readjust ECF.•To prevent nocturia, encourage patients to take diuretics in themorning.•Inadequate response to diuretic therapy:–Noncompliancewith diuretic use.–Noncompliancewith salt restriction.–Decreasedor delayed absorption of diuretic.–Decreasedrenal blood flow or GFR – increase diuretic dose to Kincrease delivery.–Addanother diuretic. For example, for patients on loop diuretics add a thiazide orK+-sparing diuretic.–Drug-druginteractions -- competes with diuretics for secretion. 
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