ELIGIBLE MEDICATIONS albuterol sulfate Airet, Proventil, Ventolin ; bitolterol mesylate Tornalate ; isoetharine Bronkometer, Bronkosol ; isoproterenol hydrochloride Isuprel ; metaproterenol sulfate Alupent, Metaprel ; pirbuterol acetate Maxair ; other beta agonists INELIGIBLE MEDICATIONS beclamethosone dipropianate Beclovent, Beconase, Vancenase, Vanceril ; cromolyn sodium Intal ; dexamethasone sodium Ddecadron Respihaler ; flunisolide Aerobid ; ipratropium bromide Atrovent ; epinephrine Primatene Mist OTC If yes, proceed to the next question IF NO, PATIENT IS NOT ELIGIBLE 5. Ask the patient or caregiver, "Would you like us to ASSIST you ; in taking the same type of medication that you ; take when you ; have an attack?" If yes, proceed to the next step NOTE: The EMT will use their own medication nebulizer and oxygen ; , because the patient's medication may be ineffective or out of date. If NO, TREAT THE PATIENT APPROPRIATELY AND TRANSPORT 6. A. If the patient is between 6 months and 2 years of age, assemble the appropriate nebulizer and fill it with the full unit dose of albuterol sulfate and full contents of a saline "squirt." Dose for Patient Care Report 2.5 mg in 6 ml saline. 742 LW A. S .Wiener, and G. I. Brancato. of Forensic Medicine, New!

Dexamethasone Decqdron ; yes 2-8 mg po sc od 4 mg ml injectable added to other medications for resistant nausea. mainstay for raised ICP, or severe liver involvement. excellent anti-emetic working at several receptors. Is sedating. substitute for other antiemetics rather than adding in.

Methods timing and procedures ; Zone 1 will be maintained by an annual application of non-selective residual herbicide applied according to label instructions and in compliance with all state and federal regulations. Zone 1 applications will not be made during periods of heavy rain or in wind greater than 10 miles per hour. Applications will be made in the early spring, typically beginning the 1st of March. They will be planned and carried out depending on weather patterns and precipitation events. Zone 1 chemical applications will be documented on the WSDOT Pesticide Application Record. Prescriptions See Appendix A, Routine Maintenance Prescriptions, Zone 1 Maintenance and beconase. The following are the various chemotherapy agents your child may receive in preparation for a bone marrow stem cell transplant. Not all of the potential side effects may occur and the toxicities vary greatly from child to child. We will let you know of the most frequent side effects and those that are rare. 1. ATG Anti-Thymocyte Globulin ; What it does: Decreases the body's ability to reject new bone marrow stem cells. May also be used to treat graft vs. host disease. Made in horses or rabbits. How it is given: Administered IV over 4-10 hours. The recipient will be premedicated with Tylenol, Benadryl, and Decadron to help prevent reactions. Potential side effects: Fever Chills Hives or other skin rashes Severe allergic reaction rare ; 2. BCNU Carmustine ; What it does: How it is given: Potential side effects.
DR. RICHARD LUTES: This is Dr. Richard Lutes, reporting from the Eighth International Myeloma Workshop in Banff, Alberta. We are discussing the final session, "Thalidomide, Mechanisms of Action and Clinical Outcomes, " and we welcome Dr. Kenneth Anderson of the Dana-Farber Cancer Institute in Boston. Good morning Dr. Anderson. To start with can you just give us your overview of thalidomide please? DR. KENNETH ANDERSON: Thalidomide is clearly a breakthrough in the therapy of multiple myeloma. Over two years ago it was used for the first time by doctors in Arkansas led by Dr. Bart Barlogie, and the observation in the clinic was that one-third of patients responded who literally responded to nothing else, in many cases having failed even two transplants. What's happened since is a flurry of activity to learn more about how to use thalidomide, to develop novel thalidomides that are even more potent that might have fewer side effects, and to rapidly move those new compounds from the bench or the laboratory to the clinic in trials with patients. DR. RICHARD LUTES: Can you give us an overview of the role of thalidomide first in refractory patients, and second then as up-front therapy? DR. KENNETH ANDERSON: Thalidomide in the initial study at the University of Arkansas achieved a response in approximately 30 percent of patients. As I mentioned earlier, many of these patients had failed high-dose therapy and were not treatable with any other conventional therapy. As is true of all the other agents we use to treat myeloma, when you use drugs earlier in the disease course, they work more effectively. Clearly tumor cells are sensitive to treatments early on after diagnosis, but they acquire drug resistance and have a more malignant phenotype with time. So thalidomide alone and together with other drugs, one of those being Decadron, has now been explored early in newly diagnosed multiple myeloma patients. At this session, Dr. Donna Weber of M.D. Anderson in Houston and Dr. Vincent Rajkumar of the Mayo Clinic each reported on the combination of thalidomide and Decadron, both in refractory patients but more importantly in up-front or newly diagnosed patients with myeloma. In the refractory setting, 40 percent to as many as half of the patients responded to thalidomide and Decadron and surprisingly, some of these patients had failed either Decadron or thalidomide alone. But fully half of such patients will respond to the combination. Even more exciting, when you use thalidomide together with Decadron in the early part of the disease course shortly after diagnosis, the response rates are much higher in the range of 70 to high as 80 percent rather than the third or 30 percent that we see in refractory disease and deltasone.

And cardiac disease. Do not use with epinephrine. Throatirritation, hoarseneu, andcoughingmayoccur. Before prescribing or administering, read product circular with package or available on request. SUPPLIED: RESPIHALER DECADRON Phosphate and RESPIHALER ProDECADRON are aerosols for oral inhalation and are supplied in aerosoiized conlainers. RESPIHALER DECADRON Phosphate and RESPIHALER ProDECADRON deliver, in the case of RESPIHALER DECADRON Phosphate, approximately 0.084 mg. of DECADRONA Dexamethasone 0.1 mg. of dexamethasone 21-phosphate as disodium. Perilymphatic Fistula in Congenital Malformations of the Inner Ear In contrast to CSF leakage, a perilymphatic fistula requires only one abnormal pathway: an interconnection of the inner ear with the tympanic cavity. In all probability, perilymph fistula and CSF leak are part of a spectrum of related disturbances of inner ear fluid homeostasis. Although separation of the two topics may be artificial pathophysiologically, it can be justified by the different clinical settings of the two problems. With CSF leakage, the cardinal clinical issues are gross fluid leakage and recurrent meningitis, whereas with perilymph fistulization, sudden or progressive hearing loss and vertigo are the primary manifestations. Much controversy surrounds the diagnosis and management of perilymphatic fistula PLF ; in children. The candidate group for exploratory tympanotomy is children with progressive or sudden SNHL. CT scan of the inner ear may demonstrate pneumolabyrinth, although this is rare Fig. 125-15 ; . Conservative surgeons have advocated exploring only children with radiographically abnormal inner ears who have a clear antecedent event of head trauma or barometric pressure change Pappas et al, 1988 ; . Others have espoused exploring all children with unexplained SNHL Parnes and McCabe, 1987; Reilly, 1989; Supance and Bluestone, 1983 ; . There is great variability in the number of fistulas "confirmed" at surgery. Pappas et al 1988 ; found only 4 fistulas in 36 ears 11% ; explored for progressive SNHL during childhood. It is important to note that 50% of these ears had radiographically malformed inner ears. By contrast, Parnes and McCabe 1987 ; found fistulas in 20 of children's ears 77% ; , only 6 of whom had inner ear anomalies radiographically. When performing a perilymph fistula exploration it is important to perform provocative maneuvers to render subtle perilymph flows more visible. These include performance of the Valsalva maneuver, using the Trendelenburg position, and compression of the jugular veins. Depending on one's point of view, many surgeons are either missing subtle or intermittent PLFs during explorations or overdiagnosing them by misinterpreting middle ear secretions or local anesthetic as perilymph. Most surgeons patch both oval and round windows with connective tissue whether or not a PLF was identified during exploration. Rather than dwell on the controversy about how many fistulas are found, the critical observer should judge the effectiveness of the therapeutic intervention by analyzing its outcome relative to the natural history of the disease. In this regard, results of PLF exploration in children have been disappointing. In one series of 36 patients, hearing was better in 3, unchanged in 21, and worse in 12 Pappas et al, 1988 ; . Similar results have been obtained in other childhood PLF series. It would be difficult to argue that these data represent a significant improvement over the natural history of the inner ear disease. Congenital progressive SNHL is often characterized by long periods of stability interspersed with periods of rapid deterioration. Even a relative improvement in hearing may occur after an episode of sudden loss. It is apparent that most children with sudden or progressive SNHL have suffered from cochlear diseases other than PLF. Examples include hereditary progressive loss, viral labyrinthitis for example, measles, mumps, cytomegalovirus ; , autoimmune inner ear disease for example, Cogan's syndrome ; , and endolymphatic hydrops. Even in the situation of highest suspicion - sudden loss triggered by head trauma in a child with radiographically malformed inner ears - only a minority of patients demonstrate oval- or round-window fistulization. Many of these children probably lose hearing as a result of internal fistulization between the endolymphatic and perilymphatic space due to deficiencies of the osseous spiral lamina rather than due to external fistulization to the middle ear. A minority of children with sudden or progressive SNHL have prominent vestibular symptoms. Results with PLF repair in the relief 13 and phenergan.
Dr. Richard Lutes: This is Dr. Richard Lutes at the 38th Annual Meeting of American Society of Clinical Oncology, Orlando, FL, May 18, 2002. We have just completed a session on clinical update in advances in the treatment of multiple myeloma. I have the pleasure of talking with Dr. Kenneth Anderson of the Dana Farber Cancer Institute, who discussed novel therapies. Welcome, Dr. Anderson. Dr. Kenneth Anderson: Thank you. Dr. Lutes: As a way of introduction to novel therapies, the drug, thalidomide, changed the way we thought about the treatment of myeloma. Could you discuss thalidomide and the impact that it had on the myeloma patient? Dr. Anderson: Surely. Thalidomide was used to treat myeloma for the first time almost four years ago, based on the fact that thalidomide inhibits new blood vessel formation and the fact that patients with myeloma have too many new blood vessels in their bone marrow. This drug was used for the first time to treat the microenvironment in the bone marrow rather than to treat the tumor cell itself. As research has subsequently shown, thalidomide and the newer thalidomide drugs, the so-called immunomodulatory drugs, not only inhibit angiogenesis, but they also directly act on the myeloma cell and alter the ability of the myeloma cell to bind and grow in the bone marrow, as well. So the new paradigm that thalidomide was a drug that targeted the host myeloma cell interaction, as well as the myeloma bone marrow, in addition to targeting the tumor cell as other conventional therapies do. Dr. Lutes: The category of drugs you discussed, the, IMiDs, how do they work? Dr. Anderson: The IMiDs are the immunomodulatory drugs, or derivatives of thalidomide. They are 1, 000 times more potent than thalidomide, and they work by inducing death of myeloma cell lines in patient cells that are resistant to the standard drugs we use to treat myeloma, so that cells that are resistant to melphalan, to Adriamycin or to Decadron are still killed by the IMiDs. In addition, they alter or inhibit the ability of the myeloma cell to bind to the bone marrow, and they stop the production of cytokines or factors in the bone marrow that are needed for the.

DEFINITION: Unwanted weight gain is an increase in body weight that is of concern to an individual. It may occur in some cancer patients as a result of the cancer itself, cancer treatment including surgery, chemotherapy, and hormone therapy ; or medications used to control the side effects of the cancer or treatment eg. steroids ; . Surgical procedures, such as ovary ablation and hysterectomy that alter menopausal status, may also predispose women to weight gain. Weight gain appears most common in breast cancer and cancers of the central nervous system CNS ; , gynecological cancers, lymphoma and Hodgkin's disease. Prevention and or treatment of unwanted weight gain in patients with cancer is important for improving quality of life, enhancing body image, facilitating patients' sense of control, and has the potential to enhance overall survival in women with breast cancer 1, 3, 4 ; . POSSIBLE CAUSES Steroid Use: Weight gain frequently results from the use of steroids, such as Decadron dexamethasone ; , prescribed for the control of nausea and or inflammation in patients with breast cancer, cancers of the CNS, lymphoma and Hodgkin's disease. Long-term use of steroids causes weight gain primarily due to an increase in energy intake resulting from an enhanced appetite. Breast Cancer and or Adjuvant Chemotherapy: In women with breast cancer, it is unclear whether weight gain is an effect of the cancer itself or the effect of cancer treatment, specifically chemotherapy and hormonal therapy, or as a result of natural or treatment-related menopause. Weight gain during adjuvant chemotherapy has been consistently reported in the past two decades and is greatest with the use of multi-agents, longer treatment lengths, and with intravenous versus oral ; administration and is greater in pre-menopausal women 1, 3 ; . Weight gain in women with breast cancer is likely multifactorial, due to the following contributing factors. The most popular but unproven theory ; is that weight gain occurs due to an increase in energy intake 1, 3 ; . This is thought to be as result of frequent eating to diminish nausea, food cravings similar to pregnancy ; , enhanced appetite with steroids used as antiemetics ; , anticipation.

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