Pharmacotherapy Handbook, 7th Edition - KSU

Contents47.48.49.50.51.Skin and Soft-Tissue Infections . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .509Surgical Prophylaxis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .522Tuberculosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .532Urinary Tract Infections and Prostatitis . . . . . . . . . . . . . . . . . . . . . . . .544Vaccines, Toxoids, and Other Immunobiologics . . . . . . . . . . . . . . . . .556SECTION 9: NEUROLOGIC DISORDERSEdited by Barbara G. Wells52.53.54.55.56.Epilepsy. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .577Headache: Migraine and Tension-Type . . . . . . . . . . . . . . . . . . . . . . . .599Pain Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .614Parkinson’s Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .629Status Epilepticus. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .637SECTION 10: NUTRITIONAL DISORDERSEdited by Cecily V. DiPiro57.58.59.60.Assessment and Nutrition Requirements . . . . . . . . . . . . . . . . . . . . . . .647Enteral Nutrition . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .655Obesity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .663Parenteral Nutrition . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .669SECTION 11: ONCOLOGIC DISORDERSEdited by Cecily V. DiPiro61.62.63.64.65.Breast Cancer . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .679Colorectal Cancer . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .689Lung Cancer . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .699Lymphomas . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .704Prostate Cancer . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .713SECTION 12: OPHTHALMIC DISORDERSEdited by Cecily V. DiPiro66. Glaucoma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .719SECTION 13: PSYCHIATRIC DISORDERSEdited by Barbara G. Wells67. Alzheimer’s Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .72768. Anxiety Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .73569. Bipolar Disorder . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .756vii

Contents70.71.72.73.Major Depressive Disorder . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .Schizophrenia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .Sleep Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .Substance-Related Disorders. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .778799814823SECTION 14: RENAL DISORDERSEdited by Cecily V. DiPiro74.75.76.77.78.Acid–Base Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .Acute Renal Failure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .Chronic Kidney Disease. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .Drug Dosing in Renal Insufficiency . . . . . . . . . . . . . . . . . . . . . . . . . . .Electrolyte Homeostasis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .839849858875881SECTION 15: RESPIRATORY DISORDERSEdited by Terry L. Schwinghammer79. Allergic Rhinitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 89780. Asthma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 90681. Chronic Obstructive Pulmonary Disease. . . . . . . . . . . . . . . . . . . . . . . 921SECTION 16: UROLOGIC DISORDERSEdited by Cecily V. DiPiro82. Benign Prostatic Hyperplasia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 93183. Erectile Dysfunction. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 93684. Urinary Incontinence. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 944APPENDICESEdited by Barbara G. dix1. Allergic and Pseudoallergic Drug Reactions. . . . . . . . . . .2. Geriatrics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .3. Drug-Induced Hematologic Disorders . . . . . . . . . . . . . . .4. Drug-Induced Liver Disease . . . . . . . . . . . . . . . . . . . . . . .5. Drug-Induced Pulmonary Disorders . . . . . . . . . . . . . . . .6. Drug-Induced Kidney Disease . . . . . . . . . . . . . . . . . . . . . .951955958962965971Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 975viii

PrefaceThis seventh edition of the pocket companion to Pharmacotherapy: A Pathophysiologic Approach, seventh edition, is designed to provide practitioners andstudents with critical information that can be easily used to guide drug therapydecision making in the clinical setting. To ensure brevity and portability, thebulleted format provides the user with essential textual information, key tablesand figures, and treatment algorithms.Corresponding to the major sections in the main text, disorders are alphabetized within the following sections: Bone and Joint Disorders, CardiovascularDisorders, Dermatologic Disorders, Endocrinologic Disorders, Gastrointestinal Disorders, Gynecologic and Obstetric Disorders, Hematologic Disorders,Infectious Diseases, Neurologic Disorders, Nutritional Disorders, OncologicDisorders, Ophthalmic Disorders, Psychiatric Disorders, Renal Disorders,Respiratory Disorders, and Urologic Disorders. Drug-induced conditions associated with allergic and pseudoallergic reactions, hematologic disorders, liverdisease, pulmonary disorders, and kidney disease appear in five tabular appendices. In the seventh edition, information on the management of pharmacotherapy in the elderly has been added as an appendix. Also in the seventhedition, chapters have been added on adrenal gland disorders and influenza.Carrying over a popular feature from Pharmacotherapy, each chapter isorganized in a consistent format: Disease state definitionConcise review of relevant pathophysiologyClinical presentationDiagnosis Desired outcome Treatment MonitoringThe treatment section may include nonpharmacologic therapy, drug selection guidelines, dosing recommendations, adverse effects, pharmacokineticconsiderations, and important drug–drug interactions. When more in-depthinformation is required, the reader is encouraged to refer to the primary text,Pharmacotherapy: A Pathophysiologic Approach, seventh edition.It is our sincere hope that students and practitioners find this book helpfulas they continuously strive to deliver highest quality patient-centered care.We invite your comments on how we may improve subsequent editions ofthis work.Barbara G. WellsJoseph T. DiPiroTerry L. SchwinghammerCecily V. DiPiroPlease provide your comments about this book, Wells et al., PharmacotherapyHandbook, seventh edition, to its Authors and Publisher by writing topharmacotherapy@mcgraw-hill.com. Please indicate the author and title ofthis handbook in the subject line of your e-mail.ix

AcknowledgmentsThe editors wish to express their sincere appreciation to the authors whosechapters in the seventh edition of Pharmacotherapy: A Pathophysiologic Approachserved as the basis for this book. The dedication and professionalism of theseoutstanding practitioners, teachers, and clinical scientists are evident on everypage of this work. The authors of the chapters from the seventh edition areacknowledged at the end of each respective Handbook chapter.x

To the ReaderBasic and clinical research provides a continuous flow of biomedical information that enables practitioners to use medications more effectively andsafely. The editors, authors, and publisher of this book have made every effortto ensure accuracy of information provided. However, it is the responsibilityof all practitioners to assess the appropriateness of published drug therapyinformation, especially in light of the specific clinical situation and newdevelopments in the field. The editors and authors have taken care torecommend dosages that are consistent with current published guidelinesand other responsible literature. However, when dealing with new andunfamiliar drug therapies, students and practitioners should consult severalappropriate information sources.xi

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SECTION 1BONE AND JOINT DISORDERSCHAP TEREdited by Terry L. Schwinghammer1Gout and HyperuricemiaDEFINITIONS The term gout describes a disease spectrum including hyperuricemia, recurrent attacks of acute arthritis associated with monosodium urate crystals inleukocytes found in synovial fluid, deposits of monosodium urate crystals intissues (tophi), interstitial renal disease, and uric acid nephrolithiasis. Hyperuricemia may be an asymptomatic condition, with an increasedserum uric acid concentration as the only apparent abnormality. A urateconcentration greater than 7.0 mg/dL is abnormal and associated with anincreased risk for gout.PATHOPHYSIOLOGY In humans, uric acid is the end product of the degradation of purines. Itserves no known physiologic purpose and is regarded as a waste product.The size of the urate pool is increased severalfold in individuals with gout.This excess accumulation may result from either overproduction orunderexcretion. The purines from which uric acid is produced originate from threesources: dietary purine, conversion of tissue nucleic acid to purine nucleotides, and de novo synthesis of purine bases. Abnormalities in the enzyme systems that regulate purine metabolism mayresult in overproduction of uric acid. An increase in the activity ofphosphoribosyl pyrophosphate (PRPP) synthetase leads to an increasedconcentration of PRPP, a key determinant of purine synthesis and thusuric acid production. A deficiency of hypoxanthine–guanine phosphoribosyl transferase (HGPRT) may also result in overproduction of uric acid.HGPRT is responsible for the conversion of guanine to guanylic acid andhypoxanthine to inosinic acid. These two conversions require PRPP as thecosubstrate and are important reutilization reactions involved in nucleicacid synthesis. A deficiency in the HGPRT enzyme leads to increasedmetabolism of guanine and hypoxanthine to uric acid and more PRPP tointeract with glutamine in the first step of the purine pathway. Completeabsence of HGPRT results in the childhood Lesch-Nyhan syndrome,characterized by choreoathetosis, spasticity, mental retardation, and markedly excessive production of uric acid. Uric acid may also be overproduced as a consequence of increasedbreakdown of tissue nucleic acids, as with myeloproliferative and lymphoproliferative disorders. Cytotoxic drugs used to treat these disorders can1

SECTION 1 Bone and Joint Disordersalso result in overproduction of uric acid due to lysis and breakdown ofcellular matter.Dietary purines play an unimportant role in the generation of hyperuricemia in the absence of some derangement in purine metabolism orelimination.About two-thirds of the uric acid produced each day is excreted in theurine. The remainder is eliminated through the GI tract after enzymaticdegradation by colonic bacteria. A decline in the urinary excretion of uricacid to a level below the rate of production leads to hyperuricemia and anincreased miscible pool of sodium urate.Drugs that decrease renal clearance of uric acid through modification offiltered load or one of the tubular transport processes include diuretics,nicotinic acid, salicylates (less than 2 g/day), ethanol, pyrazinamide,levodopa, ethambutol, cyclosporine, and cytotoxic drugs.The average human produces 600 to 800 mg of uric acid daily and excretesless than 600 mg in urine. Individuals who excrete more than 600 mg afterbeing on a purine-free diet for 3 to 5 days are considered overproducers.Hyperuricemic individuals who excrete less than 600 mg of uric acid per24 hours on a purine-free diet are defined as underexcretors of uric acid.On a regular diet, excretion of more than 1,000 mg per 24 hours reflectsoverproduction; less than this is probably normal.Deposition of urate crystals in synovial fluid results in an inflammatoryprocess involving chemical mediators that cause vasodilation, increasedvascular permeability, complement activation, and chemotactic activity forpolymorphonuclear leukocytes. Phagocytosis of urate crystals by leukocytes results in rapid lysis of cells and a discharge of proteolytic enzymesinto the cytoplasm. The ensuing inflammatory reaction is associated withintense joint pain, erythema, warmth, and swelling.Uric acid nephrolithiasis occurs in 10% to 25% of patients with gout.Predisposing factors include excessive urinary excretion of uric acid, acidicurine, and highly concentrated urine.In acute uric acid nephropathy, acute renal failure occurs as a result ofblockage of urine flow secondary to massive precipitation of uric acidcrystals in the collecting ducts and ureters. This syndrome is a wellrecognized complication in patients with myeloproliferative or lymphoproliferative disorders and results from massive malignant cell turnover, particularly after initiation of chemotherapy. Chronic urate nephropathy is causedby the long-term deposition of urate crystals in the renal parenchyma.Tophi (urate deposits) are uncommon in gouty subjects and are a latecomplication of hyperuricemia. The most common sites of tophaceousdeposits in patients with recurrent acute gouty arthritis are the base of thegreat toe, helix of the ear, olecranon bursae, Achilles tendon, knees, wrists,and hands. CLINICAL PRESENTATION Acute attacks of gouty arthritis are characterized by rapid onset of excruciating pain, swelling, and inflammation. The attack is typically monoarticular2

Gout and Hyperuricemia CHAPTER 1at first, most often affecting the first metatarsophalangeal joint (podagra),and then, in order of frequency, the insteps, ankles, heels, knees, wrists,fingers, and elbows. Attacks commonly begin at night, with the patientawakening from sleep with excruciating pain. The affected joints are erythematous, warm, and swollen. Fever and leukocytosis are common. Untreatedattacks may last from 3 to 14 days before spontaneous recovery. Although acute attacks of gouty arthritis may occur without apparentprovocation, attacks may be precipitated by stress, trauma, alcohol ingestion, infection, surgery, rapid lowering of serum uric acid by ingestion ofuric acid–lowering agents, and ingestion of certain drugs known to elevateserum uric acid concentrations.DIAGNOSIS The definitive diagnosis is accomplished by aspiration of synovial fluidfrom the affected joint and identification of intracellular crystals ofmonosodium urate monohydrate in synovial fluid leukocytes. When joint aspiration is not a viable option, a presumptive diagnosis ofacute gouty arthritis may be made on the basis of the presence of thecharacteristic signs and symptoms, as well as the response to treatment.DESIRED OUTCOME The goals in the treatment of gout are to terminate the acute attack,prevent recurrent attacks of gouty arthritis, and prevent complicationsassociated with chronic deposition of urate crystals in tissues.TREATMENTACUTE GOUTY ARTHRITIS(Fig. 1-1)Nonpharmacologic Therapy Patients may be advised to reduce their intake of foods high in purines (e.g.,organ meats), avoid alcohol, increase fluid intake, and lose weight if obese. Joint rest for 1 to 2 days should be encouraged, and local application of icemay be beneficial.Nonsteroidal Antiinflammatory Drugs Nonsteroidal antiinflammatory drugs (NSAIDs) are the mainstay of therapy because of their excellent efficacy and minimal toxicity with shortterm use. There is little evidence to support one NSAID as more efficaciousthan another, and three drugs (indomethacin, naproxen, and sulindac)have FDA approval for this indication (Table 1-1). Therapy should be initiated with maximum recommended doses for goutat the onset of symptoms and continued for 24 hours after completeresolution of an acute attack, then tapered quickly over 2 to 3 days. Acuteattacks generally resolve within 5 to 8 days after initiating therapy.3

SECTION 1 Bone and Joint DisordersContraindicationto NSAID?Acute gouty arthritisNOYESOnset of symptoms 48 hours?NONSAID of choiceYESInadequate responseNumber of jointsinvolvedOral colchicineInadequate response1 1Joint accessible toinjection?YESContraindication tosystemic gesics and joint rest / oral colchicineYESNOParenteral or oral corticosteroid / intraarticular corticosteroidFIGURE 1-1. Treatment algorithm for acute gouty arthritis. (NSAID, nonsteroidalantiinflammatory drug.)4

Gout and HyperuricemiaTABLE 1-1 CHAPTER 1Dosage Regimens of Nonsteroidal AntiinflammatoryDrugs for Treatment of Acute Gouty ArthritisGeneric NameDosage and toprofenNaproxenPiroxicamSulindac300 mg twice daily300–600 mg three to four times daily800 mg four times a day25–50 mg four times a day for 3 days, then taper to twice daily for 4–7 days75 mg four times a day500 mg twice daily for 3 days, then 250–500 mg daily for 4–7 days20 mg once daily or 10 mg twice daily200 mg twice daily for 7–10 days The most common adverse effects involve the GI system (gastritis, bleeding, and perforation), kidneys (renal papillary necrosis, reduced creatinineclearance [CLcr]), cardiovascular system (sodium and fluid retention,increased blood pressure), and CNS (impaired cognitive function, headache, dizziness). Although the risk of GI complications is relatively small with short-termtherapy, coadministration with a proton pump inhibitor should be considered in elderly patients and others at increased GI risk. NSAIDs should beused with caution in individuals with a history of peptic ulcer disease, heartfailure, uncontrolled hypertension, renal insufficiency, coronary arterydisease, or if they are receiving anticoagulants concurrently. The efficacy and safety of cyclooxygenase-2 (COX-2) selective inhibitors(e.g., celecoxib) have not been fully assessed in gouty arthritis, but they aremore costly than conventional NSAIDs and are unlikely to result in fewerGI complications because of the short duration of therapy.Colchicine Colchicine is an antimitotic drug that is highly eff

This seventh edition of the pocket companion to Pharmacotherapy: A Patho-physiologic Approach, seventh edition, is designed to provide practitioners and students with critical information that can be e