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Portosplenomesenteric venous thrombosis frequently develops in patients with Intravascular volume depletion secondary to medicine interactions purchase oxytrol 5 mg with amex leakage of necrotizing acute pancreatitis but rarely leads to medications prescribed for anxiety quality oxytrol 2.5 mg complica­ fuids in the pancreatic bed andileus with fuid-filled loops tions medicine 54 543 cheap oxytrol 2.5mg mastercard. Treatment of Acute Disease collections and necrosis may be acute (within the first 4 weeks) or chronic (after 4 weeks) and sterile or infected medicine for high blood pressure purchase oxytrol 5 mg without a prescription. Mild disease-In most patients, acute pancreatitis is a Chronic collections, including pseudocysts and walled-off mild disease ("nonsevere acute pancreatitis") that subsides necrosis, are characterized by encapsulation. The pancreas is "rested" infected necrotizing pancreatitis may complicate the course by a regimen of withholding food and liquids by mouth, of 5-10% of cases and accounts for most of the deaths. The bed rest, and, in patients with moderately severe pain or risk ofinfection does not correlate with the extent of necro­ ileus and abdominal distention or vomiting, nasogastric sis. Early fuid resuscitation (one-third of the total kocytosis, and, in some cases, shock and is associated with 72-hour fuid volume administered within 24 hours of organ failure (eg, gastrointestinal bleeding, respiratory presentation, 250-500 mL/h initially) may reduce the fre­ failure, acute kidney injury) in 50% of cases. Pain is controlled with meperidine, up to 100-150 A serious complication of acute pancreatitis is acute mg intramuscularly every 3-4 hours as necessary. Parenteral nutrition (including able alternative and, given the potential side effects of lipids) should be considered in patients who have severe meperidine, may even be preferable. Oral intake of fuid pancreatitis and ileus; glutamine supplementation appears and foods can be resumed when the patient is largely free to reduce the risk of infectious complications and mortal­ of pain and has bowel sounds (even if the serum amylase is ity. Clear liquids are given first (this step may be sterile pancreatic necrosis to infected necrosis is still con­ skipped in patients with mild acute pancreatitis), followed troversial and generally is not indicated in those with less by gradual advancement to a low-fat diet, guided by the than 30% pancreatic necrosis. Following recovery venously three times daily, then 250 mg orally twice daily) from acute biliary pancreatitis, laparoscopic cholecystec­ administered for no more than 14 days to patients with tomy is generally performed, preferably during the same sterile pancreatic necrosis has been reported in some stud­ hospital admission, and is associated with a reduced rate of ies to reduce the risk of pancreatic infection and mortality; recurrent gallstone-related complications compared with meropenem and the combination of ciprofoxacin and delayed cholecystectomy. In selected cases endoscopic metronidazole do not appear to reduce the frequency of sphincterotomy alone may be done. When rent pancreatitis associated with pancreas divisum, insertion infected necrosis is confirmed, imipenem or meropenem of a stent in the minor papilla (or minor papilla sphincter­ should be continued. In occasional cases, a fungal infection otomy) may reduce the frequency of subsequent attacks, is found, and appropriate antifungal therapy should be although complications of such therapy are frequent. The role of intravenous somatostatin in severe patients with recurrent acute pancreatitis attributed to pan­ acute pancreatitis is uncertain, and octreotide is thought to creatic sphincter of Oddi dysfunction, biliary sphincterot­ have no beneft. A small study has suggested benefit from omy alone is as effective as combined biliary and pancreatic pentoxiflline. To date, probiotic agents have not been sphincterotomy in reducing the frequency of recurrent acute shown to reduce infectious complications of severe pancre­ pancreatitis, but chronic pancreatitis may still develop in atitis and may increase mortality. Hypertriglyceridemia with acute pancre­ infammatory drugs (eg, indomethacin administered atitis has been treated with insulin, heparin, or apheresis, rectally) and aggressive hydration with lactated Ringer but the beneft of these approaches has not been proven. Severe disease-In more severe pancreatitis-particularly and rectal indomethacin has become standard practice. Risk factors for ulinastatin, and nitroglycerin, but further studies are high levels of fuid sequestration include younger age, alco­ needed. Treatment of Complications and Follow-Up in adequate urinary output, stabilization of blood pressure and heart rate, restoration of central venous pressure, and A surgeon should be consulted in all cases ofsevere acute a modest decrease in hematocrit value cannot be overem­ pancreatitis. Calcium gluconate must be given intravenously if indicates a strong possibility of a serious surgically correct­ there is evidence of hypocalcemia with tetany. Infusions of able lesion (eg, perforated peptic ulcer), exploratory lapa­ fresh frozen plasma or serum albumin may be necessary in rotomy is indicated. If the pancreatitis appears mild and cholelithiasis or shock persists after adequate volume replacement (includ­ microlithiasis is present, cholecystectomy or cholecystos­ ing packed red cells), pressors may be required. When severe pancreatitis results patient requiring a large volume of parenteral fuids, cen­ from choledocholithiasis and jaundice (serum total biliru­ tral venous pressure and blood gases should be monitored bin above 5 mg/dL [85. Endoscopic sphincterotomy nutrition for at least 7-10 days and reduces the risk of does not appear to improve the outcome of severe pancre­ multiorgan failure and mortality when started within 48 atitis in the absence of cholangitis or jaundice. A severe initial attack and group of relatively stable patients with infected pancreatic smoking also increase the risk of recurrence. The goal chronic pancreatitis following an episode of acute alcoholic is to debride necrotic pancreas and surrounding tissue and pancreatitis is 13% in 10 years and 16% in 20 years, and the establish adequate drainage. Outcomes are best if necrosec­ risk of diabetes mellitus is increased more than twofold tomy is delayed until the necrosis has organized, usually over 5 years. A "step-up" approach in of patients with recurrent acute pancreatitis; alcohol use which nonsurgical drainage ofwalled-off pancreatic necro­ and smoking are principal risk factors. When to Admit mortality and resource utilization in selected patients with necrotizing pancreatitis and confirmed or suspected sec­ Nearly all patients with acute pancreatitis should be ondary infection. Factors that affect disease progression after options, depending on local expertise. Same­ surgical drainage when infected or associated with persist­ admission versus interval cholecystectomy for mild gallstone ing pain, pancreatitis, or bile duct obstruction. Pancreatic ductleaks and fistulas may logic prevention of pancreatitis after endoscopic retrograde require endoscopic or surgical therapy. Half of the deaths occur within the first 2 weeks, usually from multiorgan failure. Chronic or intermittent epigastric pain, steator­ ure is associated with a mortality rate of at least 30%, and if rhea, weight loss, abnormal pancreatic imaging. The risk of death doubles when both idiopathic, genetic, autoimmune, recurrent and organ failure and infected necrosis are present. General Considerations dicted by a scoring system based on five factors during the index admission: eating less than a solid diet at discharge; Chronic pancreatitis occurs most often in patients with nausea, vomiting, or diarrhea at discharge; pancreatic alcoholism (45-80% of all cases). The risk of chronic pan­ necrosis; use of antibiotics at discharge; and pain at dis­ creatitis increases with the duration and amount of alcohol charge. Male sex, an alcohol etiology, and severe acute consumed, but pancreatitis develops in only 5-10% ofheavy disease are risk factors. Tobacco smoking is a risk factor for idiopathic holic pancreatitis but can be reduced by repeated, regularly chronic pancreatitis and has been reported to accelerate scheduled interventions to eliminate alcohol consumption progression of alcoholic chronic pancreatitis. Attacks may last only a few hours or as tropical Africa and Asia, tropical pancreatitis, related in long as 2 weeks; pain may eventually be almost continuous. Laboratory Findings globulinemia (IgG in particular), often with autoantibod­4 Serum amylase and lipase may be elevated during acute ies and other autoimmune diseases, and is responsive to attacks; however, normal values do not exclude the diagno­ corticosteroids. Tye 1 autoimmune pancreatitis (or sim­ vated owing to compression of the bile duct. Glycosuria ply "autoimmune pancreatitis") is a multisystem disease may be present. Excess fecal fat may be demonstrated on characterized by lymphoplasmacytic sclerosing pancreati­ chemical analysis of the stool. Pancreatic insufficiency this on biopsy, associated bile duct strictures, retroperitoneal generally is confrmed by response to therapy with pancre­ fibrosis, renal and salivary gland lesions, and a high rate of atic enzyme supplements; the secretin stimulation test can relapse after treatment. It is the pancreatic manifestation of be used if available (and has a high negative predictive fac­ IgG -related disease. Type 2 ("idiopathic duct4 -centric tor for ruling out early acute chronic pancreatitis), as can chronic pancreatitis") affects the pancreas alone and is detection of decreased fecal chymotrysin or elastase lev­ characterized by duct-centric pancreatitis on biopsy, lack els, although the latter tests lack sensitivity and specificity. Accurate diagnostic tests are available 10% and 30% of cases of chronic pancreatitis are idio­ for the major trypsinogen gene mutations, but because of pathic, with either early onset (median age 23) or late onset uncertainty about the mechanisms linking heterozygous (median age 62). In many raise suspicion of pancreatic cancer ("tumefactive chronic cases, chronic pancreatitis is a self-perpetuating disease pancreatitis"). After many years, chronic pain may normal in patients with so-called minimal change pancre­ resolve spontaneously or as a result of surgery tailored to atitis. Clinical Findings culi in the main pancreatic duct and lobularity with honey­ combing of the pancreatic parenchyma. Symptoms and Signs imaging features of autoimmune pancreatitis include dif­ Persistent or recurrent episodes of epigastric and left upper fuse enlargement of the pancreas, a peripheral rim of quadrant pain are typical. The pain results in part from hypoattenuation, and irregular narrowing of the main impaired inhibitory pain modulation by the central ner­ pancreatic duct. During attacks, tology, imaging, serology, other organ involvement, and tenderness over the pancreas, mild muscle guarding, and response to corticosteroid therapy. Pancreatic cancer develops in 4% of patients after 20 years; the risk may relate Immediate-Release Capsule to tobacco and alcohol use. In patients with hereditary Nonenteric-coated pancreatitis, the risk of pancreatic cancer rises after age 50 years and reaches 19% by age 70 years (see Chapter 39). Treatment Correctable coexistent biliary tract disease should be Enteric-coated minimicrospheres treated surgically. Medical Measures Creon 12,000 12,000 60,000 38,000 A low-fat diet should be prescribed. Alcohol is forbidden Creon 24,000 24,000 120,000 76,000 because it frequently precipitates attacks.

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Specim ens Supernatantisthen transferred to medicine you cant take with grapefruit purchase oxytrol 2.5 mg with amex anotherplastic m ustbe stored refrigerated overnightat20C to medicine quizlet buy genuine oxytrol on line 80 C treatment venous stasis buy oxytrol 5 mg mastercard. A com plete24-hoururinespecim en iscollected withorwithout10g boricacidtom aintainpH <7 medications herpes order generic oxytrol. PrecisionandBias If collected withoutpreservative uine should be refrigeratedduring thecollectionperiod. E ach laboratory should ensure that Afterm easuring the totalvolum e,a thoroughly appropriate internalqualitycontroland externalquality m ixedaliquot(fi 10m l)isstoredfrozenat-200C. Careshould betaken to ensurean appropriately Any laboratory consistently unable to tim ed, com plete 24-hour collection because an m eetthefollowing criteriaandwhichcannotchangetoa incorrectly tim ed sam ple isthe largestsource of error superiorassayshouldrefersam pleselsewhere. Q ueenslandhealthpathologyservices:R oyalBrisbane glasssurfaces,and can be rapidly degraded by plasm a H ospital,Testslist,collectiondetails2001 proteasesintoim m unoreactivefragm entsduring freezing andthawing of thespecim en. Annalsof If steroidsarerequiredwithinthis24hourperiod, InternalM edicine1999;130:759-771 preferreddrug isDexam ethasone. CortisolDeficiency Procedure SynacthenStim ulationof Cortisol-(short) Cannulatethepatientandtakebaselinesam ple(0 TestforAdrenalI nsufficiency m in)forcortisol. Screening tests for an aldosterone producing tum our include evaluation of hypertencsion and V alues between 0. Tietztextbookof Clinicalbiochem istry3rd • Serum potassium editionDutyBiochem istsM anual,Departm entof clinicalbiochem istry,R oyalPerthhospital,Sydney, • U rinarypotassium Australia,2001 To dem onstraterenallossesof potassium in the presence of hypokalaem ia the patientshould be on at R ecom m endations least 120 m m ol/l of sodium for 3 days before A. Should becarried outunderthesupervision and investigation,sincealow sodium intakem aynorm alize recom m endation of a consultant. Pleasediscusswiththerelevantlaboratorybefore Sam ples SpotU rine sendingthespecim ens. Should becarried outunderthesupervision and Thesubjectisawakenedat0600handkeptinan recom m endation of a consultant. Thesubjectthen Aldosterone is the m ajor m ineralocorticoid assum esasupineposition,and2L of isotonicsaline,0. Blood isdrawn from the non-I V infusion arm forplasm aaldosteroneand electrolytesdeterm inationat Procedure 1200h the testis carried outin the ward under Potassium shouldbefi 3. Patientsm ayhavefluidsbutotherwiseshouldbe O bserve patientone hour prior to discharge. Should becarried outunderthesupervision and Confirmation recom m endation of a consultant. Sam plesshould Salineinfusiontest(2L isotonicsalineover4hours)andmeasureplasmaaldosterone be sentto the relevantlaboratory for analysis. Plasmaaldosterone>10ng/dl Plasmaaldosterone<10ng/dl O r Plasmaaldosteronelevel or 24hurinaryaldosterone>10-14µg/d 5-10ng/dl 24hoururinaryaldosterone withurinesodium >250nmol/d <8µg/d R eferences rd 1. Diagnostic Borderline E xcludeprimary DutyBiochem istM anual,R oyalPerthH ospital, hyperaldosteronism Australia,2001 L ocalization 2. If an uprightblood specim en is to be collected,the subjectshould be in an uprightposition O sm olalityshouldbeanalyzedonlybyanosm om etre. Specim enshouldbestoredfrozeninanairtightcontainer Transportthe sam ples to the laboratory as andarestableforup to2yat-200C. Thistestisto establishthediagnosisof diabetes Specim ensshould notbe acidified with strong m ineral insipidus in a patientwith polyuria,polydipsia,and acids,suchashydrochloricacid. Aftercentrifugation atroom tem perature,the 0 Contraindications plasm aisrem ovedandfrozenat-20C. If theurineosm olalityis>800m O sm ol/K g water reeze thaw cycles should be avoided because of the withoutexogenous1-desam ino-8-D argininevasopressin possibleactivationof prorenin. Atthetim eof collection,blood should notbe Before com m encing the testhypothyroidism, chilled or placed on ice because irreversible cortisol deficiency and osm otic diuresis m ust be cryoactivation of prornin can occur,leading to falsely excluded. Serum osm olalityis 275-295m osm ol/K g U rineosm olality >600m osm ol/K g Itisim portantto m onitorvitalsignsduring the U rine/serum osm olalityratio >2 dehydrationprocedure. Thepatientwillbeconsidered ashaving norm al If weightlossexceeds2K g (or5% inchildren)or posterior pituitary reserve and further testing is not the clinical condition deteriorates,the testm ust be indicated. Because of this,patientsm ustnotbeallowedtodrinkfreelyafter Itisim portantto m onitorvitalsignsduring the com pletionof thetestif theyhaverespondedtothedrug. If weightlossexceeds2K g (or5% inchildren)or the clinical condition deteriorates, the testm ustbe E conom izationof resources stopped. The following patients can be exem pted from following thecom pletetestprotocolafterassessm entof W aterdeprivation testisnotindicated if serum PosteriorPituitaryR eserveinthefollowing m anner. Basalinvestigations If theserum osm olalityis>300m osm /K g water Serum osm olality inapatientsuspectedof having diabetesinsipidus,orin U rineosm olality very sm all children, testing can be done without (O btainedsim ultaneouslyonrising orassoonas subjecting thepatienttoaperiodof dehydration. Procedure Draw a sam ple of blood (1m l) for m easured the laboratorym ustbegiven noticein advance osm olalityandsodium whentheplateauisreached. The of com m encem entof test/specim encollection laboratorywillinform thistotheward. E nsure availability of a ward environm entin Afterblood hasbeen collected,inject5unitsof which the patientcan be observed and in which the aqueous vasopressin subcutaneously or adm inister patientdoesnothaveaccesstoanywater,including hand intranasaldesm opressinacetateinthefollowing doses. O ne hour later collect urine for m easured Inchildrenthetestshouldbecarriedoutinthedaytim e osm olality and blood sam ple form easured osm olality undersupervision. If thereisno definitechangein urineosm olality Priorto fasting (before 0700 hours-7. Should becarried outunderthesupervision and Insipidus of serum) >50% to >300 recom m endation of a consultant. Specim ensshouldbetransportedtothelaboratory 0 oniceandcentrifugedat4C within30m inof collection. R eferenceranges Serum neonatem aybeaslow as266 m O sm ol/kg H 2O childandadult 275-295m O sm ol/kg H 2O >60yr 280-301 m O sm ol/kg H 2O U rinerandom 50-1200depending onthefluidintake R eferences 1. Biochem istrym anual,Departm entof Clinical Biochem istry,W estm eadH ospitalforchildren, Australia 2002. Draw 4-hour and 8-hour cortisols; run 8-hour first and 4-hour may not be indicated. Diagnose High-Dose Dexamethasone Suppression Protocol For Determination of Pituitary-Dependent vs. Observe for decrease in appetite, 7–10 days into loading water intake <60 cc/kg/day, dose with no adverse effects or vomiting, diarrhea or lethargy. Supplement with prednisone as <1 µg/dL >5 µg/dL stimulation tests and observe for adverse needed. Treat Trilostane (Vetoryl) Dosing and Monitoring* Treatment of Canine Hyperadrenocorticism Day 1 Start trilostane treatment. Clinical signs of hypoadrenocorticism Recheck at one month Stop treatment for 7 days. As with any diagnosis or treatment, you should use clinical discretion with each patient based on a complete evaluation of the patient, including history, physical examination and complete laboratory data profile. With respect to any drug therapy or monitoring program, you should refer to product inserts for a complete description of dosages, indications, interactions and cautions. The complete urinalysis is an important part of the minimum database and without it we are likely going to take much longer to get to the root of the problem. The complete urinalysis is relevant across a wide variety of patient visit types and provides invaluable information for other organ systems including: • Kidney health • Lower urinary conditions • Liver disease • Diabetes mellitus and diabetic ketoacidosis • Hydration status • Other endocrine disease as Cushing’s disease (hyperadrenocorticism) • Acid-base status • Hemolytic diseases the complete urinalysis comes in three parts: • the physical examination • the chemical examination • microscopic examination of the sediment the physical examination the physical examination consists of visualizing the collected urine and recording the color and clarity of the sample. Change in urinary color from its normal appearance – light yellow to amber – indicates the presence of pigments in the urine which can indicate lower urinary tract disease or systemic disease. Change in urine clarity is most often due to the presence of red blood cells, white blood cells, or crystals in the urine. The chemical examination the chemical examination of the urine uses dipsticks to provide semi-quantitative measurement of various urine chemicals that serve as important markers for major disorders or conditions. There are numerous suppliers of reagent strips —nearly all intended for use with human urine. To properly perform a urine chemistry evaluation, follow these steps: • Use a fresh urine sample or, if refrigerated, use a sample returned to room temperature. The chemistry will be looking at these parameters: pH— the pH of urine is an index of acid-base balance but is not a reliable indicator of blood pH. Erythrocytes, free hemoglobin, methemoglobin, or myoglobin may be a source of heme. Red blood cells should be confirmed with sediment exam to help differentiate between hematuria and pigmenturia (erythrocytes may lyse in very alkaline or dilute urine). Excessive bilirubinuria in a dog or any bilirubinuria in a cat is an indication to evaluate serum bilirubin concentrations. However, there is a poor correlation between increased levels of urobilinogen and either hepatobiliary disease or hemolysis in dogs and cats.

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Light chain components may be depos­ ited in tissues as amyloid medicine clip art order oxytrol online pills, resulting in kidney failure with albuminuria and a vast array of systemic symptoms treatment 10 buy oxytrol 2.5mg amex. Myeloma patients are prone to treatment whiplash discount 2.5mg oxytrol with amex recurrent infections for a number ofreasons treatment alternatives purchase cheapest oxytrol and oxytrol, including neutropenia, the underproduc­. Bone pain, often in the spine, ribs, or proximal tion of normal immunoglobulins and the immunosuppres­ long bones. Monoclonal paraprotein by serum or urine protein prone to infections with encapsulated organisms such as electrophoresis or immunofixation. The most common presenting complaints are those related to anemia, bone pain, kidney disease, and infection. General Considerations ent as a pathologic fracture, especially of the femoral neck Multiple myeloma is a malignancy of hematopoietic stem or vertebrae. Patients may also come to medical attention cells terminally differentiated as plasma cells characterized because of spinal cord compression from a plasmacytoma by infltration of the bone marrow, bone destruction, and or the hyperviscosity syndrome (mucosal bleeding, vertigo, paraprotein formation. The diagnosis is established when nausea, visual disturbances, alterations in mental status, monoclonal plasma cells (either kappa or lambda light hypoxia). Many patients are diagnosed because of labora­ chain restricted) in the bone marrow (any percentage) or as tory findings of hypercalcemia, proteinuria, elevated sedi­ a tumor (plasmacytoma), or both, are associated with end­ mentation rate, or abnormalities on serum protein organ damage (such as bone disease [lytic lesions, osteope­ electrophoresis obtained for symptoms or in routine nia], anemia [hemoglobin less than 10 g/dL {100 g/L}], screening studies. L}], or kidney injury [creatinine greater than 2 mg/ Examination may reveal pallor, bone tenderness, and dL {176. Sixty percent or more clonal plasma cells in the bone related to neuropathy or spinal cord compression. Fever marrow or a serum free kappa to lambda ratio of greater occurs mainly with infection. Laboratory Findings plasma cells in the bone marrow, a serum paraprotein level of 3 g/dL (30 g/L) or higher, or both, without plasma cell­ Anemia is nearly universal. The absence of rouleaux formation, however, mas) that may cause spinal cord compression or other sof­ excludes neither multiple myeloma nor the presence of a tissue problems. The neutrophil and platelet counts are excessive osteoclast activation mediated largely by the usually normal at presentation. Approximately 15% of patients will have no demonstrable the paraproteins (monoclonal immunoglobulins) paraprotein in the serum because their myeloma cells pro­ secreted by the malignant plasma cells may cause problems duce onlylight chains and not intact immunoglobulin, and in their own right. Very high paraprotein levels (either IgG the light chains pass rapidly through the glomerulus into or IgA) may cause hyperviscosity, although this is more the urine. Overall, the paraprotein is of bone pain or other symptoms and complications related IgG (60%), IgA (20%), or light chain only (15%) in multiple to the disease. The initial treatment generally involves at a myeloma, with the remainder being rare cases ofIgD, IgM, minimum an immunomodulatory agent, such as thalido­ or biclonal gammopathy. In sporadic cases, no paraprotein mide or lenalidomide, or a proteasome inhibitor, such as is present ("nonsecretory myeloma"); these patients have bortezomib, in combination with moderate or high-dose particularly aggressive disease. The major side effects oflenalidomide are the bone marrow will be infltrated by variable num­ neutropenia and thrombocytopenia, venous thromboem­ bers of monoclonal plasma cells. Bortezomib has the morphologically abnormal often demonstrating multi­ advantages of producing rapid responses and of being nucleation and vacuolization. The major side effect marked skewing of the normal kappa-to-lambda light of bortezomib is neuropathy (both peripheral and auto­ chain ratio, which will indicate their clonality. Many nomic), which is largely ameliorated when given subcuta­ benign processes can result in bone marrow plasmacytosis, neously rather than intravenously. A common regimen for but the presence of atypical plasma cells, light chain restric­ initial treatment is lenalidomide, bortezomib, and dexa­ tion, and effacement of normal bone marrow elements methasone. Imaging Carflzomib, a second-generation proteasome inhibitor, produces responses in patients for whom bortezomib treat­ Bone radiographs are important in establishing the diagno­ ment fails and does not cause neuropathy. Lytic lesions are most commonly seen in some inhibitor, ixazomib, is available for relapsed disease. The radionuclide bone scan is not useful in detecting bone After initial therapy, many patients under age 80 years lesions in myeloma, since there is usually no osteoblastic are consolidated with autologous hematopoietic stem cell component. In the evaluation of patients with known or transplantation following high-dose melphalan. Differential Diagnosis posttransplant maintenance therapy but at the expense of an elevated rate of second malignancies. Vertebral collapse with its attendant pain defined as bone marrow monoclonal plasma cells less than and mechanical disturbance can be treated with vertebro­ 10% in the setting of a paraprotein (serum M-protein less plasty or kyphoplasty. Hypercalcemia and hyperuricemia than 3 g/dL [30 g/L]) and the absence of end-organ dam­ should be treated aggressively and immobilization and age. The bisphosphonates (pamidronate gresses to overt malignant disease in a median of one 90 mg or zoledronic acid 4 mg intravenously monthly) decade. Multiple myeloma, smolder­ and are an important adjunct in this subset of patients. However, long-term bisphosphonates, linemia (which is commonly seen in cirrhosis). Myeloma patients with oliguric or anuric renal failure at Patients with smoldering myeloma treated with lenalido­ diagnosis should be treated aggressively with chemo­ mide (an immunomodulatory agent) and dexamethasone therapy and considered for plasma exchange (to reduce take longer to progress to symptomatic myeloma and live the paraprotein burden), as return of renal function can longer than when simply observed. An update on the use oflenalidomide for the the outlook for patients with myeloma has been steadily treatment of multiple myeloma. The International Staging System for myeloma relies on two factors: beta 2-microglobulin and albumin. Infiltration of bone marrow by plasmacytic is established when beta-2-microglobulin is greater than lymphocytes. General Considerations at chromosome l4q32 (such as the finding of t[4;14] or t[l4;16]) or multiple copies of the lq2l-23 locus. Abnor­ Waldenstrom macroglobulinemia is a syndrome of IgM malities of chromosome l7p also confer a particularly poor hypergammaglobulinemia that occurs in the setting of a prognosis. When to Refer paraprotein, and many clinical manifestations of the dis­ All patients with multiple myeloma should be referred to a ease are related to this macroglobulin. Symptoms and Signs Hospitalization is indicated for treatment of acute kidney this disease characteristically develops insidiously in failure, hypercalcemia, or suspicion of spinal cord com­ patients in their 60s or 70s. Patients usually present with pression, for certain chemotherapy regimens, or for hema­ fatigue related to anemia. Mucosal and gastrointes­ tinal bleeding is related to engorged blood vessels and platelet dysfunction. An update in treatment options for multiple paraprotein may also cause symptoms of cold agglutinin myeloma in nontransplant eligible patients. Allogeneic stem cell transplantation in multi­ On examination, there may be hepatosplenomegaly or ple myeloma: immunotherapy and new drugs. Treatment options for relapsed and refractory volume by 50-100% due to the presence of the paraprotein. The clinical relevance and management istically infltrated by the plasmacytic lymphocytes. Overall survival and competing risks of death in is over four times that ofwater, and marked symptoms usu­ patients with Waldenstrim macroglobulinaemia: an analysis ally arise when the viscosity is over six times that of water. Waldenstrom macroglobulinemia: prognosis and tion of paraprotein and serum viscosity. General Considerations Patients with marked hyperviscosity syndrome (stupor, Amyloidosis is anuncommon condition whereby a protein coma, pulmonary edema) should be treated on an emer­ abnormally deposits in tissue resulting in organ dysfunc­ gency basis with plasmapheresis. The propensity of a protein to be amyloidogenic is a patients can be managed with periodic plasmapheresis consequence of disturbed translational or posttranslational alone. The input of amyloid protein into tissues rituximab (375 mg/m2 intravenously weekly for 4-8 weeks) far exceeds its output, so amyloid build up inexorably pro­ has significant activity. However, a word of caution: the ceeds to organ dysfunction and ultimately organ failure IgM often rises first after rituximab therapy before it falls. Combination therapy is recommended for advanced dis­ Amyloidosis is classified according to the type of amy­ ease (see Table 39-ll). Bortezomib, thalido­ and renal failure type (beta-2-microglobulin, not fltered mide, lenalidomide, and bendamustine have also been out by dialysis membranes [Abeta-2M]). Autologous hemato­ frther classified as localized (amyloid deposits only in a poietic stem cell transplantation is reserved for relapsed or single tissue type or organ) or, most common, systemic refractory patients.

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The increase platelets (and also red blood cells and white blood neutropenic patient is increasingly vulnerable to medications used for fibromyalgia buy 5mg oxytrol visa infection cells) in patients with refractory aplastic anemia medicine man dr dre purchase oxytrol 2.5mg amex. By its nature symptoms emphysema oxytrol 2.5mg without prescription, despite very low stable neutrophil levels; they seem to medications given for uti buy genuine oxytrol line myelosuppressive cytotoxic chemotherapy causes neutro­ respond adequately to infections and infammatory stimuli penia in a predictable manner. Clinical Findings cyclic neutropenia periodically oscillate (usually in 21-day Neutropenia results in stomatitis and in infections due to cycles) between normal and low, with infections occurring gram-positive or gram-negative aerobic bacteria or to during the nadirs. Fever in neutropenic A variety of bone marrow disorders and nonmarrow patients should always be initially assumed to be of infec­ conditions may cause neutropenia (Table 13-12). Treatment isolated neutropenia is most often due to an idiosyncratic reaction to a drug, and agranulocytosis (complete absence Treatment of neutropenia depends on its cause. Potential of neutrophils in the peripheral blood) is almost always causative drugs should be discontinued. In these cases, examination of the factors (flgrastim or sargramostim) help facilitate neutro­ bone marrow shows an almost complete absence of granu­ phil recovery after offending drugs are stopped. This myeloid growth factor administration (daily or every other marrow fnding is also seen in pure white blood cell apla­ day) is effective at dampening the neutropenia seen in sia, an autoimmune attack on marrow granulocyte precur­ cyclic or congenital neutropenia. Neutropenia in the presence of a normal bone leads to repeated bacterial infections, splenectomy has marrow may be due to immunologic peripheral destruc­ been the treatment of choice, but sustained use of myeloid tion (autoimmune neutropenia), sepsis, or hyersplenism. Patients with autoimmune neutropenia often supports the diagnosis of autoimmune neutropenia. Felty respond briefy to immunosuppression with corticoste­ syndrome is an immune neutropenia associated with sero­ roids and are best managed with intermittent doses of positive nodular rheumatoid arthritis and splenomegaly. Splenectomy is held in reserve for Severe neutropenia may be associated with clonal disorders failure to respond to corticosteroids and myeloid growth of T lymphocytes, often with the morphology of large factors. The tropenia is an uncommon presentation of hairy cell neutropenia associated with large granular lymphoprolif­ erative disorder may respond to therapy with either low­ dose methotrexate or cyclosporine. Enteric gram-negative bacteria Congenital are of primary concern and ofen empirically treated with Dyskeratosis congenita fuoroquinolones or third or fourth-generation cephalospo­ Fanconi anemia rins. For protracted neutropenia, fungal infections are prob­ Cyclic neutropenia lematic and empiric coverage with azoles (fuconazole for Large granular lymphoproliferative disorder yeast and voriconazole, itraconazole, or posaconazole for Hairy cell leukemia molds) or echinocandins is recommended. The neutropenia Myelodysplasia Non-bone marrow disorders following myelosuppressive chemotherapy is predictable Drugs: sulfonamides, chlorpromazine, procainamide, and is partially ameliorated by the use of myeloid growth penicillin, cephalosporins, cimetidine, methimazole, factors. For patients with acute leukemia undergoing intense phenytoin, chlorpropamide, antiretroviral medications, chemotherapy or patients with solid cancer undergoing rituximab high-dose chemotherapy, the prophylactic use of antimicro­ Aplastic anemia bial agents and myeloid growth factors is recommended. When to Refer Pure white cell aplasia Hypersplenism Refer to a hematologist if neutrophils are persistently and Sepsis unexplainably less than 1000/mcL (1. When to Admit Felty syndrome Neutropenia by itself is not an indication for hospitaliza­ Systemic lupus erythematosus tion. Most patients with febrile neutropenia require hospitalization to treat infection. Antimicrobial prophylaxis and outpatient Primary myelofibrosis management of fever and neutropenia in adults treated for Essential thrombocytosis malignancy: American Society of Clinical Oncology clinical Chronic myeloid leukemia practice guideline. Management of sepsis in neutropenic patients: cell lines, most prominently the red blood cells. True erythrocytosis, with an elevated red blood cell Myeloproliferative disorders are due to acquired clonal mass, should be distinguished from spurious erythrocyto­ abnormalities of the hematopoietic stem cell. Primary poly­ stem cell gives rise to myeloid, erythroid, and platelet cells, cythemia (polycythemia vera) is a bone marrow disorder qualitative and quantitative changes are seen in all of these characterized by autonomous overproduction of erythroid cell lines. Clinical Findings ever, these disorders are grouped together because they may evolve from one into another and because hybrid A. Sixty percent of patients are men, and the median age at presentation is 60 years. Thrombosis is the most common complication of polycythemia vera and the major cause of morbidity and death in this disorder. Thrombosis appears to be related both to increased blood viscosity and abnormal platelet function. The hallmark of polycythemia vera is a hematocrit (at sea level) that exceeds 54% in males or 51% in females. General Considerations blood count is usually elevated to 10,000-20,000/mcL and Polycythemia vera is an acquired myeloproliferative disor­ the platelet count is variably increased, sometimes to der that causes overproduction of all three hematopoietic counts exceeding 1,000,000/mcL. White Count Hematocrit Platelet Count Red Cell Morphology Polycythemia vera Nor I t Nor I N Essential thrombocytosis Nor I N tt N Primary myelofibrosis Nod or l t J or Nor I Abn Chronic myeloid leukemia tt N N orl N Abn, abnormal; N, normal. A positive family history should lead to investiga­ basophilia and eosinophilia are frequently present. The absence of a mutation should lead the clinician to other myeloproliferative disorders, essential thrombocyto­ question the diagnosis. The bone marrow is hypercellular, with panhyperplasia of Polycythemia vera should be differentiated from other all hematopoietic elements, but bone marrow examination is myeloproliferative disorders (Table 13-14). Abnormal red blood cell morphology and nucleated increased circulating red blood cell mass. Iron defciency may red blood cells in the peripheral blood are seen in myelof­ also result from chronic gastrointestinal blood loss. Essential thrombocytosis is suggested when the may lower the hematocrit to the normal range (or lower), platelet count is strikingly elevated. Treatment Vitamin B12 levels are strikingly elevated because of the treatment of choice is phlebotomy. Patients for at presentation, microcytosis, hypochromia, and poikilocy­ whom phlebotomy is problematic (because of poor venous tosis may result from iron deficiency following treatment access or logistical reasons) may be managed primarily with by phlebotomy. Differential Diagnosis iron supplementation, as this can thwart the goals of a phle­ Spurious polycythemia, inwhich an elevated hematocrit is botomy program. A diet low in iron also is not necessary but due to contracted plasma volume rather than increased red will increase the intervals between phlebotomies. Maintain­ cell mass, may be related to diuretic use or may occur with­ ing the hematocrit at normal levels has been shown to out obvious cause. A secondary cause ofpolycythemia should be suspected Occasionally, myelosuppressive therapy is indicated. There is evidence that causes of polycythemia include hypoxia and smoking; car­ reduction ofthe platelet count to less than 600,000/mcL will boxyhemoglobin levels may be elevated in smokers reduce the risk of thrombotic complications. The usual dose is 500-1500 mg/day orally, adjusted to keep platelets less than 500,000/mcL without Table 13-1S. In a randomized study comparing best available ther­ Carboxyhemoglobin: smoking apy with ruxolitinib, treatment with ruxolitinib was Kidney lesions associated with greater beneft for both hematocrit control Erythropoietin-secreting tumors (rare) without phlebotomy (60%) and splenic volume reduction Abnormal hemoglobins (rare) (38%). The risk of thrombosis Low-dose aspirin (75-81 mg/day orally) has been rises with age. Venous thromboses may occur in unusual shown to reduce the risk of thrombosis without excessive sites such as the mesenteric, hepatic, or portal vein. Some bleeding, and should be part of therapy for all patients patients experience erythromelalgia, painful burning ofthe without contraindications to aspirin. Allopurinol 300 mg hands accompanied by erythema; this symptom is reliably orally daily may be indicated for hyperuricemia. Bleeding, typically mucosal, is less mine therapy with diphenhydramine or other H1-blockers common and is related to a concomitant qualitative platelet and, rarely, selective serotonin reuptake inhibitors are used defect. Prognosis An elevated platelet count is the hallmark of this disorder, Polycythemia is an indolent disease with median survival and may be over 2,000,000/mcL (2000 x 109/L) (Table of over 15 years. The bone marrow shows increased numbers of mega­ Patients with polycythemia vera should be referred to a karyocytes but no other morphologic abnormalities. Philadelphia chromosome is absent but should be assayed by molecular testing of peripheral blood for the bcr! When to Admit fusion gene in all suspected cases to differentiate the disor­ Inpatient care is rarely required. The clinical and laboratory evaluation ofthe patient ondary causes of an elevated platelet count. Treatment Essential thrombocytosis isanuncommon myeloprolifera­ tive disorder ofunknown cause in which marked prolifera­ Patients are considered at high risk for thrombosis if they tion of the megakaryocytes in the bone marrow leads to are older than 60 years, have a leukocyte count of 11 x 109/L elevation of the platelet count. The risk of thrombosis others in these patients promises to advance the under­ can be reduced by control of the platelet count, which standing of this disorder.

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