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Though oculomucocutaneous involvement is most common generic 100mg lady era mastercard womens health zeitschrift, possible additional sites include the respiratory tract discount lady era 100 mg online menopause urinary tract infections, oropharynx 100mg lady era otc menstrual tent, esopha- gus, gastrointestinal tract, and anal and urogenital regions. Conjunctivitis on examination warrants an immediate ophthalmology consult, because serious complications including blindness can occur. Urology input, evaluation or treat- ment for urinary tract anomaly or infection, and social work involvement is premature, because the etiology for his penile abnormality is likely mucosal erosion, not infection or trauma. He should, however, be closely monitored in an intermediate care unit at the onset. Some patients have low N-acetyltransferase activity in the liver rendering them “slow acetylators. Stevens-Johnson syndrome in a boy with macrolide-resistant Mycoplasma pneumoniae pneumonia. Recurrence and outcomes of Stevens-Johnson syndrome and toxic epidermal necrolysis in children. Describe how a patient’s age affects the presentation and outcome of bacterial meningitis. Considerations This teen has the typical triad of meningitis symptoms: fever, headache, and a stiff neck; his altered mental status is another often-seen finding. Other causes of mental status changes include viral meningoencephalitis, trauma, intentional or accidental ingestion, and hypoglycemia. Of these alternatives, only viral meningoencephalitis would likely explain the fever and stiff neck. Other organisms, including Citrobacter sp, Staphylococcus sp, group D streptococci, and Candida sp, are rare. Infants at increased risk for meningitis include low-birth-weight and preterm infants, and those born to mothers with chorioamnionitis after a prolonged rupture of the amniotic membranes, or by traumatic delivery. Clinical symptoms in infants are nonspecific and not the typical triad of headache, fever, and stiff neck. Instead, infants may have thermal instability (often hypothermia), poor feeding, emesis, seizures, irritability, and apnea. Infants may have a bulging fontanelle, and they demonstrate generalized hyper- or hypotonicity. Bacterial meningitis in older children is usually caused by Streptococcus pneu- moniae or Neisseria meningitidis; vaccination has essentially eliminated Haemophilus influenzae type B. Other rarer causes in this age group include Pseudomonas aeru- ginosa, Staphylococcus aureus, Staphylococcus epidermidis, Salmonella sp, and Listeria monocytogenes. The incidence of pneumococcal meningitis is 1 to 6 cases per 100,000 children per year, more commonly occurring in the winter. It is an encapsulated pathogen; children with a poorly functioning or absent spleen are at higher risk. Children with sickle cell disease have an infection incidence 300 times greater than in unaffected children. Neisseria meningitidis colonizes the upper respiratory tract in approximately 15% of normal individuals; carriage rates up to 30% are seen during invasive disease outbreaks. Family members and day care workers in close contact with children having meningitis are at 100- to 1000-fold increased risk for contracting disease. A plethora of other bacterial, viral, fungal, and mycobacterial agents can cause meningitis. The classic symptoms of meningitis seen in older children and adults may be accompanied by mental status changes, nausea, vomiting, lethargy, restlessness, ataxia, back pain, Kernig and Brudzinski signs, and cranial nerve palsies. Approxi- mately one-quarter to one-third of patients have a seizure during the illness course. Patients with N meningitidis can have a petechial or purpuric rash (purpura ful- minans), which is associated with septicemia. Patients with septicemia due to N meningitidis often are gravely ill and may or may not have associated meningitis. Cerebrospinal fluid analysis includes Gram stain and culture, white and red blood cell counts, and protein and glucose analysis. Typical bacterial meningitis find- ings include an elevated opening pressure, several hundred to thousands of white blood cells with polymorphonuclear cell predominance, and elevated protein and decreased glucose levels. Treatment strategies vary by patient age, likely pathogens, and local resistance pat- terns. In the neonatal period, ampicillin often is combined with a third-generation cephalosporin or an aminoglycoside to cover infections caused by group B Streptococcus, E coli, and L monocytogenes. Neonates in an intensive care unit may be exposed to nosocomial infections; prevalent pathogens in that nursery must be considered. In some locales, more than half of the pneumococcal isolates are intermediately or highly penicillin resistant; 5% to 10% of the organisms are cephalosporin resis- tant. Thus, in suspected pneumococcal meningitis, a third-generation cephalosporin combined with vancomycin is often recommended. The most common long-term sequela is hearing loss (up to 30% of patients with pneumococcus); patients with bacterial meningitis usually have a hearing evaluation at the conclusion of antibi- otic treatment. Mental retardation, neuropsychiatric and learning problems, epi- lepsy, behavioral problems, vision loss, and hydrocephalus are less commonly seen. The child with sickle cell disease (Case 13) has an immune deficiency due to splenic auto-infarction and a higher incidence of infection due to encapsulated (pneumococcus) organisms. These children also are prone to stroke which may present with acute onset of neurologic symptoms similar to those of meningitis. Meningitis due to chronic condition such as tuberculosis may present with failure to thrive (Case 10). Which of the following is the most appropriate next step in the management of this patient? The irritable, fussy infant has a heart rate of 170 beats/min and respiratory rate of 40 breaths/min. The anterior fon- tanelle is full, but he has no nuchal rigidity; the rest of the examination is unremarkable. On examination, he is alert and oriented, but he has nuchal rigidity and a positive Brudzinski sign. Which of the following is the most likely organism respon- sible for this patient’s clinical presentation? Neisseria meningitidis can present as meningococcemia with purpura and shock; in some cases patients will also have meningitis. A course of oral antibiotics, or a single dose of ceftriaxone, is not sufficient to treat meningitis or septicemia. The child described in this case has a history of sickle cell disease likely causing functional asplenia. Because of his asplenia, he is at increased risk of infection with encapsulated bacteria.
There is an increased level of clot t ing fact or s in pregn an cy order generic lady era canada womens health magazine, an d this along wit h ven ou s st asis are the t wo f a c t o r s t h a t i n c r e a s e the r i s k o f D V T i n a p r e g n a n t w o m a n f i v e f o l d purchase lady era 100mg mastercard breast cancer kobe 9. E n d o the - lial damage is part of Virchow’s triad (st asis trusted 100 mg lady era pregnancy lingerie, hypercoagulabilit y, and endothe- lial damage) that cont ribut es t o t h rombosis. It t ypically does not play a role during the pregnancy, but rather in the postpartum period when delivery, especially if surgical, may have caused some vascular damage. The most common side effect of long-term heparin use in pregnancy is osteoporosis, usually not apparent unless on the agent for at least a month. The mechanism is thought to be overactive osteoclast activity as well as decreased osteoblast activity. American T horacic Society documents: an official American Thoracic Society/ Society of Thoracic Radiology Clinical Practice Guideline—evaluation of sus- pected pulmonary embolism in pregnancy. Most likely diagnosis: Preeclampsia wit h severe feat ures Immediate next step: The highest priority must be to improve oxygenation. Sufficient oxygen must be provided to raise the O saturation >94%, and if 2 the patient is tiring, ventilator support may be required. Know the clinical presentation and diagnostic criteria for four categories of hypertensive disorders of pregnancy. Know the serious sequelae of severe features of preeclampsia, including pulmonary edema. Understand the management of preeclampsia with severe features at the pret erm and t erm gest at ions. Co n s i d e r a t i o n s The patient is nulliparous, which is a risk factor for preeclampsia. She has preeclampsia with severe features based on any one of t h ree crit eria: blood pres- sure, elevated liver function tests, and likely pulmonary edema. The physical exam and an urgent portable chest x-ray can help to assess for cardiomyopathy, pulmonary embolism, or asthma. Stabilization of maternal status has priority over fetal status; however, there should not be undue delay to evaluate the fetal status: fet al h ear t r at e pat t er n and ult rasound for fet al weight, and amniot ic fluid measurement. Deciding whether to deliver a preeclamptic patient with severe features depends on the risk to maternal/ fetal well being, the stability of the patient, and the gestational age. In the face of pulmonary edema, delivery must be enacted, since the pregnant woman’s life is in immediate jeopardy. In t he face of marked prematurit y, some severe features such as mildly elevated but st able liver funct ion test s may be observed carefully wit hout delivery. T h e management of this patient includes magnesium sulfate for seizure prophylaxis and delivery. In the absence of proteinuria, hypertension and one of the following findings may suffice: t hrombocyt openia, impaired liver funct ion t est s, renal insufficiency, pulmo- nary edema, cerebral disturbances, or visual impairment. Up to 1/ 3 of those who are thought to have gestational hypertension are later found to have preeclampsia. Preeclampsia is characterized by hypertension and proteinuria; less commonly, there is absence of proteinuria but evidence of vasospastic disease via other end- organ manifestations (see Table 16– 1). An elevated blood pressure is diagnosed with a systolic blood pressure at or > 140 mm H g or diastolic blood pressure at or > 90 mm H g. Proteinuria is usually based on timed urine collection, defined as equal to or greater than 300 mg of protein in 24 hours, although a P/ Cr ratio ≥ 0. W it h severe vasospasm t o t he brain, headache or visual disturbances can occur. Chronic hypertension includes preexisting hypertension or hypertension that develops prior to 20 weeks’gestation. A patient with chronic hyper- tension is at risk for developing preeclampsia and, if this develops, her diagnosis is labeled as superimposed preeclampsia; this diagnosis is made on the basis of new onset of severe and uncontrollable hypertension, or new onset proteinuria, or a severe fea- ture (Table 16– 2). Eclampsia occurs when the patient with preeclampsia develops convulsions or seizures, but can occur without elevated blood pressure or proteinuria. Pa t h o p h ysio lo g y The underlying pathophysiology of preeclampsia is vasospasm and “leaky vessels,” but its origin is unclear. It is cured only by termination of the pregnancy, and the disease process almost always resolves after delivery. Vasospasm and endothelial damage result in leakage of serum between the endothelial cells and cause local hypoxemia of tissue. Clin ic a l Eva lu a t io n Patients are usually unaware of the hypertension and proteinuria, and typically the presence of symptoms indicates severe disease. H ence, one of the important roles of prenat al care is to identify patients with hypertension and proteinuria prior to severe disease. Complicat ions of preeclampsia include placent al abrupt ion, eclamp- sia (wit h possible int racerebral hemorrhage), coagulopat hies, renal failure, hepat ic subcapsular hemat oma, hepat ic rupt ure, and ut eroplacent al insufficiency. Fet al gr owt h r est r ict ion, p oor Ap gar scor es, an d fet al acid osis are also m or e oft en seen. Risk factors for preeclampsia include nulliparit y, ext remes of age, African-Amer- ican race, personal h ist ory of severe preeclampsia, family h ist ory of preeclampsia, ch r on ic h yp er t en sion, ch r on ic r en al d isease, obesit y, ant iph osph olipid syn dr ome, diabetes, and multifetal gestation. Patients with chronic hypertension may sometimes already have mild proteinuria, so it is import ant to est ablish a baseline to later document superimposed preeclampsia (substantial increase in proteinuria). Also one should document any sudden increase in weight (indicating possible edema). O n physical examinat ion, serial blood pressures should be checked along with a urinalysis. Fet al testing (such as biophysical profile) is also usually performed to evaluate uteroplacental insufficiency. Management Aft er the diagnosis of preeclampsia is made, t he management will depend on the gestational age of the fetus and the severity of the disease (see Table 16– 3 and Figure 16– 1 for one management scheme). Gestational hypertensive or pre- eclamptic patients without severe features can be observed and delivered at term (37 weeks), and magnesium sulfate use is individualized. Chronic hypertensive patients who are well controlled an d u n complicat ed can be obser ved an d d eliver ed at 38 to 39 weeks. W h en severe feat ur es complicat e pr eeclampsia or super imposed preeclampsia, the risks of the preeclampsia must be weighed against the risk of prematurit y. W hat are the immediate threats to maternal status, how stable is the patient, and can these t hreat s be ameliorated? W hat are the immediate threats to fetal status, how stable is the fetus, and can these threats be ameliorated? If < 34 weeks’ gestation, can delivery be safely delayed for 48 hours to allow corticosteroids to have maximum efficacy? W hat is the natural history of the severe feature and does it seem to be worsening rapidly? Observation of a patient with severe features should be performed in a tertiary center, sin ce the r isks t o bot h the woman an d the fet u s are subst ant ial. With an unstable patient, delivery is always warranted regardless of gestational age.
For patients being treated for hematologic malignancies purchase discount lady era line breast cancer 49ers gear, palifermin [Kepivance] order lady era 100mg without a prescription menstruation rituals ancient, a chemoprotective agent and keratinocyte growth factor cheap lady era 100 mg mastercard womens health 10k, can decrease the severity of stomatitis. Diarrhea By injuring the epithelial lining of the intestine, anticancer drugs can impair absorption of fluids and other nutrients, thereby causing diarrhea. Diarrhea can be reduced with oral loperamide, a nonabsorbable opioid that slows gut motility by activating local opioid receptors. Nausea and Vomiting Nausea and vomiting are common sequelae of cancer chemotherapy. These responses, which result in part from direct stimulation of the chemoreceptor trigger zone, can be both immediate and dramatic and may persist for hours or even days. You should appreciate that nausea and vomiting associated with chemotherapy are much more severe than with other medications. Whereas these reactions are generally unremarkable with most drugs, they must be considered major and characteristic toxicities of cytotoxic drugs. These drugs offer three benefits: (1) reduction of anticipatory nausea and vomiting, (2) prevention of dehydration and malnutrition secondary to frequent nausea and vomiting, and (3) promotion of compliance with chemotherapy by reducing discomfort. The regimen of choice for patients taking highly emetogenic drugs consists of aprepitant [Emend], dexamethasone, and a serotonin antagonist, such as ondansetron [Zofran]. The use of antiemetics for chemotherapy-induced nausea and vomiting is discussed in Chapter 64. Other Important Toxicities Alopecia Reversible alopecia (hair loss) results from injury to hair follicles. Hair loss begins 7 to 10 days after the onset of treatment and reaches maximal loss in 1 to 2 months. In fact, for many cancer patients, alopecia is second only to vomiting as their greatest treatment-related fear. For patients who choose to wear a hairpiece or wig, one should be selected before hair loss occurs. Hairpieces are tax deductible as medical expenses and are covered by some insurance plans. To some degree, hair loss can be prevented by cooling the scalp while chemotherapy is being administered. Cooling causes vasoconstriction and thereby reduces drug delivery to hair follicles. Unfortunately, scalp cooling is uncomfortable, causes headache, and creates a small risk for cancer recurrence in the scalp (because drug delivery is reduced). Reproductive Toxicity The developing fetus and the germinal epithelium of the testes have high growth fractions. As a result, both are highly susceptible to injury by cytotoxic drugs, especially the alkylating agents. Risk is highest during the first trimester, and hence chemotherapy should generally be avoided during this time. However, after 18 weeks of gestation, risk appears to be very low: according to a 2012 report in Lancet, exposure during this time does not cause neurologic, cardiac, or any other fetal abnormalities. Drug effects on the ovaries may result in amenorrhea, menopausal symptoms, and atrophy of the vaginal epithelium. Hyperuricemia Hyperuricemia is defined as an excessive level of uric acid in the blood. Hyperuricemia is especially common after treatment for leukemias and lymphomas (because therapy results in massive cell kill). The major concern with hyperuricemia is injury to the kidneys secondary to deposition of uric acid crystals in renal tubules. In patients with leukemias and lymphomas, in whom hyperuricemia is likely, prophylaxis with allopurinol is the standard of care. Local Injury From Extravasation of Vesicants Certain anticancer drugs, known as vesicants, are highly chemically reactive. These drugs can cause severe local injury if they make direct contact with tissues. Vesicants are administered intravenously, usually into a central line (because rapid dilution in venous blood minimizes the risk for injury). Extreme care must be exercised to prevent extravasation because leakage can produce high local concentrations, resulting in prolonged pain, infection, and loss of mobility. Severe injury can lead to necrosis and sloughing, requiring surgical débridement and skin grafting. Because of the potential for severe tissue damage, vesicants should be administered only by clinicians specially trained to handle them safely. Unique Toxicities In addition to the toxicities discussed previously, which generally apply to the cytotoxic drugs as a group, some agents produce unique toxicities. For example, a number of drugs can cause peripheral sensory neuropathy, manifesting as numbness or tingling in the fingers and toes and around the mouth and throat. Neuropathy may impede activities of daily living, such as buttoning clothing, writing, or just holding things. Anthracyclines such as daunorubicin and doxorubicin can cause serious injury to the heart. Carcinogenesis Along with their other adverse actions, anticancer drugs have one final and ironic toxicity: these drugs, which are used to treat cancer, have caused cancer in some patients. Cancers caused by anticancer drugs may take many years to appear and are hard to treat. Making the Decision to Treat From the preceding discussion of toxicities, it is clear that cytotoxic anticancer drugs can cause great harm. Given the known dangers of these drugs, we must ask why such toxic substances are given to sick people at all. The answer lies with the primary rule of therapeutics, which states that the benefits of treatment must outweigh the risks. That is, although the toxicities of the anticancer drugs can be significant, the potential benefits (cure, prolonged life, palliation) justify the risks. There are patients whose chances of being helped by chemotherapy are remote, whereas the risk for serious toxicity is high. Because the potential benefits for some patients are small and the risks are large, the decision to institute chemotherapy must be made with care. Before a decision to treat can be made, the patient must be given some idea of the benefits the proposed therapy might offer. For treatment to be justified, there should be reason to believe that at least one of these benefits will be forthcoming. If a patient cannot be offered some reasonable hope of cure, prolonged life, or palliation, it would be difficult to justify treatment. The most important factors for predicting the outcome of chemotherapy are (1) the general health of the patient and (2) the responsiveness of the type of cancer the patient has. General health status is assessed by measuring performance status, frequently using the Karnofsky Performance Scale (Table 82. A Karnofsky score of less than 40 indicates the patient is debilitated and not likely to tolerate the additional stress of chemotherapy. Accordingly, patients with a low Karnofsky rating should not receive anticancer drugs—unless their cancer is known to be especially responsive.
Put another way lady era 100 mg low cost pregnancy or period, the result of phosphorylation is like flipping a switch lady era 100 mg without prescription womens health professionals, turning it on or turning it off lady era 100mg free shipping menopause dry skin. For example, certain regulatory proteins, when phosphorylated, activate signaling pathways that increase cell proliferation and cell survival. Accordingly, if we prevent phosphorylation with a kinase inhibitor, we can shut down the signaling pathway and thereby inhibit proliferation and promote apoptosis (programmed cell death). The other four drugs—erlotinib, gefitinib, afatinib, and lapatinib—are small molecules that work inside the cell to inhibit tyrosine kinase directly. The drug is approved for refractory colorectal cancer and for carcinoma of the head and neck. As noted, these receptors, which help regulate cell growth, are overexpressed in certain cancers, including those of the colon and rectum. The drug may be added to an irinotecan-based regimen (if the cancer has progressed despite irinotecan treatment), or it may be used alone (in patients who cannot tolerate irinotecan). Cetuximab, in combination with radiation, is approved for initial treatment of locally or regionally advanced squamous cell carcinoma of the head and neck. In addition, the drug can be used for recurrent or metastatic cancers that have progressed despite treatment with a platinum-based regimen. Manifestations include rapid-onset airway obstruction, hypotension, shock, loss of consciousness, myocardial infarction, and cardiopulmonary arrest. Severe reactions can happen with any infusion, but most (90%) occur with the first infusion. If a severe reaction develops, cetuximab should be discontinued immediately and never used again. Acne-like rash, mainly on the face and upper torso, develops in 88% of patients and is severe in 12%. Severe rash has led to Staphylococcus aureus sepsis and abscesses that require incision and drainage. Sunlight can exacerbate dermatologic reactions, and hence patients should limit sun exposure, use a sunblock, and wear protective clothing. Very rarely, cetuximab has been associated with interstitial lung disease, characterized by inflammation, scarring, and hardening of the lungs. One case of fatal interstitial pneumonitis with pulmonary edema has been reported. Whether cetuximab is truly the cause of these lung disorders has not been established. Cetuximab can cross the placenta, but whether it causes fetal harm has not been studied in humans. Panitumumab Panitumumab [Vectibix] is a monoclonal antibody similar to cetuximab with respect to mechanism, indications, and adverse effects. The principal difference between the drugs is that panitumumab is a fully human antibody, whereas cetuximab is not. Because panitumumab is a fully human antibody, severe infusion reactions are less frequent than with cetuximab (1% vs. As a result, gefitinib is restricted to patients enrolled in a medical trial in the United States. Ocular effects—amblyopia, conjunctivitis, eye pain, and corneal erosion or ulceration—occur infrequently. If respiratory symptoms develop, gefitinib should be interrupted and the patient evaluated. Gefitinib can harm the developing fetus and hence should not be used by pregnant women. In laboratory animals, the drug decreased the number of live births, increased neonatal mortality, and reduced fetal weight. Oral bioavailability is 60% in the absence of food and nearly 100% in the presence of food. Hepatotoxicity, manifesting as asymptomatic elevation of liver transaminases, occurs in some patients. The drug can also cause ocular disorders, including corneal perforation, corneal ulceration, and abnormal eyelash growth. In animal studies, erlotinib caused fetal death and abortion and hence should not be used during pregnancy. These are characterized by blistering or exfoliating lesions as well as keratitis of the eye. Five of these drugs are available: imatinib, dasatinib, bosutinib, ponatinib, and nilotinib. The other drugs—dasatinib, bosutinib, ponatinib, and nilotinib—are active against all but one of these resistant subclones and hence can be effective even in patients who no longer respond to imatinib. Because of clear superiority, imatinib had displaced interferon alfa as the initial treatment of choice. Imatinib may be continued as long as there is no evidence of disease progression and as long as side effects remain tolerable. Imatinib is also approved for myelodysplastic/myeloproliferative diseases, aggressive systemic mastocytosis, acute lymphoblastic leukemia, dermatofibrosarcoma protuberans, hypereosinophilic syndrome, chronic eosinophilic leukemia, and unresectable or metastatic malignant gastrointestinal stromal tumor, a rare form of stomach and intestinal cancer. The disease begins with a chronic phase, progresses through an accelerated phase, and ends with the blast crisis phase. The underlying cause is a genetic abnormality known as the Philadelphia chromosome, which is produced by translocation of genetic material between chromosomes 9 and 22. This enzyme phosphorylates, and thereby activates, as-yet unidentified regulatory proteins, which in turn inhibit apoptosis and stimulate cell proliferation. After 18 months, disease progression was stopped in 92% of imatinib users, compared with 74% of those getting interferon. Long-term follow-up is needed to determine how long responses to imatinib will last and whether imatinib prolongs survival. The elimination half-lives of imatinib and its major active metabolite are 18 hours and 40 hours, respectively. Common reactions include nausea, vomiting, diarrhea, rash, headache, fatigue, fever, and musculoskeletal complaints, including muscle cramps, muscle pain, and arthralgia. Fluid retention occurs in 52% to 68% of patients and may lead to pleural effusion, pericardial effusion, pulmonary edema, or ascites. Neutropenia and thrombocytopenia develop often, posing a risk for infection and bleeding. Accordingly, complete blood counts should be obtained weekly during the first month of treatment, biweekly during the second month, and periodically thereafter. Hepatotoxicity, indicated by severe elevations of transaminases or bilirubin, develops in 1.