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Other diagnostic modalities quality 100 mg caverta, such as magnetic resonance imaging and ultrasonography buy caverta 100 mg low price, can often provide the same diagnostic information as X- ray studies and carry no known risk to the fetus or embryo. Until the end of the second trimester, diagnostic techniques such as cystoscopy and sigmoidoscopy may be per- formed safely (Pentheroudakis and Pavlidis, 2006). Most surgical oncology techniques can be used during pregnancy to treat life- threatening disease, especially if they do not involve the pelvis or pelvic organs (Miller and Bloss, 1995). Ovaries can generally be removed after 10 weeks gestational age (8 weeks postconception) without apparent adverse effects on pregnancy. However, prog- estational agents should be utilized if oophorectomy is necessary prior to this time (Gilstrap and Cunningham, 1996; Pentheroudakis and Pavlidis, 2006; Yazigi and Cunningham, 1990). Most antineoplastic agents employed in chemotherapy have the capability to interfere with normal cell growth (hyperplasia, hypertrophy, and migration) in the embryo. Thus they are potentially teratogenic and may cause fetal growth retardation and congenital abnormalities. In one review of 163 pregnancies exposed to antineoplastic drugs in the first trimester, the frequency of congenital anomalies was 25 percent for polytherapy chemotherapeutic regimens and 17 percent for single-agent exposure (Doll et al. The frequency of malformations in 131 pregnancies with second-trimester exposure was 1. Hence it would be expected that exposures to antineoplastic agents after the period of embryogenesis (second and third trimesters of pregnancy) carry little risk to the fetus other than fetal growth retardation (Gilstrap and Cunningham, 1996; Yazigi and Cunningham, 1990). Antineoplastic agents may also have long-term or delayed effects, such as sterility or carcinogenesis for the child exposed prenatally (Box 7. For the benefit of the patient, some treatments (for example, for acute leukemia) should begin as soon as the diagno- sis is made, including the first trimester (Koren et al. Finally, there is a risk to the fetus from spread of the maternal cancer by transplacen- tal metastasis. It is well documented that certain cancers may spread to the developing fetus, yielding a grave fetal prognosis (Read and Platzer, 1981). Malignant melanoma is the most common cancer to metastasize to the fetus and placenta (Anderson et al. Management and treatment of specific types of cancers are discussed under Special Considerations below. Specific chemotherapeutic agents, considered below, can be divided into several classes: alkylating agents, antibiotics, antimetabolites, plant alka- loids, and miscellaneous (Boice, 1986). Antineoplastic agents can also be classified as cycle-specific and cycle-nonspecific agents. Cycle-specific agents (antimetabolites, antibiotics, and plant alkaloids) arrest cell division only during specific phases of the replication cycle. In contrast, cycle-nonspecific agents (alkylating agents) are cytotoxic during all phases of cell replication (Caliguri and Mayer, 1989). These agents act by transferring alkyl groups to such biological substrates as nucleic acids and proteins. Summary of 16 different reports of 22 infants born to busulfan- exposed patients found two infants with major congenital anomalies (2/22, 9. Subsequent reports of two exposed pregnancies resulted in normal neonates (Norhaya et al. They also reported that six (14 per- cent) of 44 infants born to women who received an alkylating agent (30 different reports) had major congenital anomalies. Experimental animal studies also report an increased frequency of congenital anomalies with exposure to busulfan during gestation. This drug is also used to treat cancers of the bladder, cervix, colorectum, endometrium, Ewing’s sarcoma, head and neck, lymphomas, kidney, lung, osteosar- coma, pancreas, and trophoblastic tumors. In addition, cyclophosphamide is efficacious in combination with other agents for the treatment of Ewing’s sarcoma, lymphomas, osteosarcoma, and trophoblastic tumors. Several studies of cyclophosphamide metabo- lism in in vitro cultures with rat embryos showed that the compound must be bioacti- vated by a monofunctional liver oxygenase system in order to be teratogenic (Fantel et al. The morphologic changes found in vitro were very similar to those seen in vivo (Greenway et al. There is no doubt that this agent produces skeletal and central nervous system anom- alies in rats (Chaube et al. Available human data are minimal and include three case reports and one case series. A set of twins comprising one normal infant and one malformed twin exposed in utero was reported. The malformed twin had multiple congen- ital abnormalities and subsequently developed thyroid cancer and neuroblastoma (Zemlickis et al. In another case report, a fetus with multiple anomalies (cleft palate, absent thumbs, and multiple eye defects) was born to a mother who was treated with cyclophosphamide in the first trimester (Kirshon et al. A growth-retarded infant with bilateral absence of the big toe, cleft palate, and hypoplasia of the fifth digit was born to a mother who received cyclophosphamide throughout pregnancy (Greenberg and Tanaka, 1964). No ill effects have been reported in association with second and third trimester exposure to cyclophosphamide (Matalon et al. Ten normal infants were reported following cyclophosphamide therapy during the first trimester (Blatt et al.
Her anxiety resolved generic caverta 50 mg otc, which was particularly useful as she made plans for her wedding buy 100 mg caverta visa. But we worked on her food plan and tried a modified elimination diet of cutting out dairy, refined carbohydrates, alcohol, and gluten. Together with the boosted progesterone, the modified elimination diet resolved Lucinda’s bloating completely. Five years of birth control pill use is associated with a 90 percent reduction in future ovarian cancer. You need B vitamins, especially vitamins B1, B2, and B6, to keep your neuroendocrine system working as an ally. In Menstrual Syndrome and Progesterone Therapy, she claimed that 83 percent of her treated patients experienced total relief. In both, progesterone was taken in whopping doses: 400 mg twice per day in one study, and 300 mg four times per day in the other. I found five randomized trials extolling the virtues of the chasteberry tree and decided to give it a try. Within one month, my period returned to arriving every twenty-eight days, and I was feeling calmer. Since women lose ovarian response to chasteberry as they age, if you don’t respond to this herb within six weeks, I recommend starting progesterone as a cream, gel, or pill, under the direction of your doctor. However, the active component of wild yam, diosgenin, can be converted into progesterone in a lab, but not in the human body. Not surprisingly, a randomized trial of wild yam cream versus placebo for menopausal symptoms showed no difference in symptoms or 35 progesterone levels. Step 3: Bioidentical Progesterone Some women are at the point in their ovarian lives where chasteberry isn’t an option: because they are in late perimenopause or menopause, their ovaries can no longer respond. I’ll tell you: many menopausal women have symptoms of low progesterone and are reluctant to use the official “hormone replacement therapy,” as they should be. Since chasteberry will not work for them, I recommend trying a small dose of progesterone cream. Bioidentical progesterone is biochemically the same as the progesterone you make in your ovaries. Rubbing 1/4 teaspoon (about the size of a dime) into your arms where they’re hairless and the skin is thin, for fourteen to twenty-five nights per month, is often enough to relieve the symptoms of low progesterone. There are three randomized trials demonstrating the efficacy of progesterone cream for women with symptoms of low progesterone, such as hot flashes. One examined a dose of 20 mg a day, and when it came to hot flashes, 83 percent in the cream group experienced fewer flashes (versus 19 percent in the placebo group), but several of the women experienced vaginal bleeding. Another trial looked at a dosage of 32 mg per day, and found that the progesterone cream raised serum levels but did not change hot flashes, mood, or sexual drive. Needless to say, this isn’t helping my marriage, and things are slowly falling apart. Donna describes fluid retention and lousy sleep before her period, no libido, and no energy to run or practice yoga. Treatment protocol: Donna has classic symptoms of low progesterone, including retained fluid, heavier periods, insomnia, poor self-soothing and decreased stress resilience. We started her on progesterone cream, 20 mg per night rubbed into the inner surface of her upper arms. Results: Within four weeks, the progesterone cream had decreased her insomnia, menstrual flow, and bloating. After eight weeks, Donna reported dramatic changes that not only improved her life but also positively impacted everyone around her. For the first time in years, she told me that she felt home again in her body, embodied and in control. She felt motivated to get back into yoga and running and possessed the mettle to cope with her daughters again. When little things happened, she didn’t fly off the handle, but managed them with grace and ease. I often find that small doses of progesterone are the small hinges that swing big doors for perimenopausal women. Taken orally, it is identical to the progesterone you’ve always made while cycling. A word of caution: use Prometrium, not Provera (medroxyprogesterone acetate), the most common progestin, or synthetic form, of progesterone. Many physicians prescribe progestins to patients suffering from irregular periods, fibroids, and/or heavy bleeding.
The Vaughan-Williamsscheme is based onwhether drugs pro- duce block in oneormore of a few sites on the cell membrane cheap 100mg caverta with mastercard, but the Sicilian Gambit takes into account a host of additional actions 50 Chapter 2 of antiarrhythmic drugs—the typeand degree of blockadeofchan- nels order caverta 100 mg, antagonistic and agonistic effects on receptors, effects on the sodium–potassium pump, the time constants of binding to cellular sites, effects on second messengers, and the afﬁnity for binding on the basisofwhether the cell is in an active or inactive state. Digoxin Relative potency of block: Low Moderate High A=Activated state blocker =Agonist =Agonist/Antagonist I = Inactivated state blocker Figure 2. Effects of each drug onchannels, receptors, and pumps are shown, as are someoftheclinical effects. Introduction to antiarrhythmic drugs 51 Two major differences exist between the Vaughan-Williams schemeand the Sicilian Gambitapproach. First, the Sicilian Gambit is far more thorough than the Vaughan-Williams systemindescrib- ing the precise actionsofantiarrhythmic drugs. Second, inasmuch as each drug is essentially in its own class (since notwo drugs are exactly alike in all the ways listed), the Sicilian Gambit is notatrue classiﬁcation system. It is, in fact, useful to have a complete tabulation of all known effects of antiarrhythmic drugs. Such a table allowsonetoeasily compare the recognized similarities and differences among drugs. Further, when the mechanisms of arrhythmias have become more precisely delin- eated, precise knowledgeofindividual drugs may helpinformu- lating more accurate guesses as to effective pharmacologic therapy (which was a speciﬁcgoal in devising the Sicilian Gambit), although it islikely to be always true that nearly identical patients with nearly identical arrhythmias often respond differently to the same drug. However, because the Sicilian Gambit is not a true classiﬁcation system, it does not offer much help to the average clinicianinlearn- ing aboutorcommunicating aboutantiarrhythmic drugs. Es- pecially for the nonexpert, the Vaughan-Williams system, with all its limitations, remains the most useful meansofcategorizing an- tiarrhythmic drugs;it is the system that will be used throughoutthis book. Yet, because of their varied effects on the sodium channel and the potassium channel, drugs assigned to Class I can behave very differently from oneanother. The major clinical features, electrophysiologic properties, and adverse effects of Class I antiarrhythmic drugs are summarizedinthe accompanying tables. Unfortunately, they are also moderately effective in causing both major varieties of side effects—end-organ toxicity and proarrhythmias. Quinidine Quinidine is the D-isomer of the antimalarial quinine, a drug that was noted to be effective in the treatmentofpalpitationsaslong 55 56 Chapter 3 Figure 3. Quinidine itself was recognized as an effective antiarrhythmic agent in the early twentieth century. Clinical pharmacology Quinidine isadministered orally as one of three salts (quinidinesul- fate, quinidine gluconate, or quinidine polygalacturonate). All three forms of the drug have beenmade available because some patients tolerate one salt better than another. Approximately 80–90% of the sulfate preparationis absorbed after oral administration,and peak plasma concentrations are reachedwithin 2 hours. The gluconate and polygalacturonate preparations are absorbedmore slowly and less completely than the sulfate formulation. Quinidine is 80–90% protein bound in the circulation and has a large volumeofdistribu- tion. The concentration of the drug is 4–10 times higher in the heart, liver, and kidneys thanit is in the circulation. Its elimination half-life is 5–8 hours but may be prolongedinpatients with congestive heart failure or in the elderly. Electrophysiologic effects Quinidine blocks the sodium channel and slows the rate of depo- larization of the actionpotential. Its effects on the potassium channels result in prolongation of the actionpotential and, therefore, of the refractory period. Like all drugs that prolong refractoriness, quinidine cancause early afterdepolar- izations(and thus torsades de pointes) in susceptible individuals. Hemodynamic effects Quinidine blocks the α-adrenergic receptors, which can lead to pe- ripheral vasodilation and reﬂex sinustachycardia. The effects tend to be minimal when the drug is given orally but can be profound with intravenousadministration. Therapeutic uses Quinidine is moderately effective in treating both atrial and ven- tricular tachyarrhythmias. Approximately 50% of patients treated with quinidine for atrial ﬁbrillation remain in sinus rhythm af- ter 1 year. Thus, quinidine has Class I antiarrhythmic drugs 59 beenused to treat virtually all varieties of reentrantsupraventricular tachyarrhythmias. Quinidine is effective in suppressing premature ventricular com- plexes and nonsustained ventricular tachycardias, butbecause of the proarrhythmic potential of quinidine(and most other antiarrhyth- mic agents), these arrhythmias shouldnot be treated excepttosup- press signiﬁcantsymptoms. For the same reason,quinidine should not be used to treat sustained ventricular tachycardia without the protection of an implantable deﬁbrillator. Adverse effects and interactions Symptomatic side effects occur in 30–50% of patients taking quini- dine, and the drug must be discontinuedin20–30% of patients be- cause of toxicity. Ingeneral, if diarrhea occurs, the drug should be discontinued,because the diarrhea is usually not adequately con- trolledwith medication and the resultant electrolyte imbalances may exacerbate the very arrhythmias that are being treated.