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Associate Professor, University of Texas Rio Grande Valley School of Medicine
Histologically and immunophenotypically women's health clinic fayetteville ar buy raloxifene with paypal, metastases usually resemble their primary tumors at least focally; it is therefore always worthwhile to review slides from a putative primary tumor whenever possible women's health and fitness tips generic 60 mg raloxifene overnight delivery. Inflammatory demyelinating disorders are characterized by myelin loss with relative preservation of axons; this finding is often accompanied by abundant foamy macrophages and perivascular lymphocytes womens health 7 supplements that melt fat buy 60mg raloxifene amex. Classic radiographic examples of myelin disorders are not generally biopsied menopause 60 discount raloxifene 60 mg otc, but when clinical and/or radiologic data are unusual or ambiguous, neurosurgery may be recommended to obtain a tissue sample. Historically, several subtypes have been described, including relapsing-remitting, secondary progressive, primary progressive, acute monophasic (Marburg disease), and acute tumefactive. Radiographically, chronic inactive plaques are hypointense on T1 and diffusion-weighted images; plaques with active inflammation are hyperintense on T2 and show postcontrast enhancement. Although the rim of enhancement around the demyelinative lesion may be incomplete at the cortical side (forming a horseshoe-shaped profile that would be highly unusual in a neoplasm), this feature is not robust enough for conclusive diagnosis; consequently, such lesions, although uncommon, are often biopsied. Mitotic activity among astrocytes and macrophages may be brisk, but nuclear atypia should be minimal. Symptoms include headache, fever and vomiting, followed by weakness, ataxia, and visual and sensory loss with progression to stupor and seizures. This clinicoradiographic pattern is characteristic enough that biopsy is not always performed. Nevertheless, when obtained, biopsy material shows perivenous demyelination with axonal sparing, mononuclear infiltrates, macrophages, activated microglia, and occasional petechial hemorrhages. Although biopsy is uncommonly undertaken, histology of the cord shows leptomeningeal and perivascular lymphocytic infiltrates, foamy macrophages, widespread myelin loss, and axonal dystrophy of the lateral columns. Patients experience 3 to 6 months of progressive neurologic symptoms that reflect the anatomic distribution of the lesions, which favor the subcortical and deep cerebral white matter, cerebellum, brainstem and, rarely, the spinal cord. Ultrastructurally, the papovavirus particles exhibit a "stick and ball" or "spaghetti and meatballs" pattern. Also noted within and around these lesions are pseudoneoplastic astrocytes with atypical nuclei; these cells do not appear to produce or contain virus particles, and should not be mistaken for astrocytoma. Diagnosis may be confirmed through immunohistochemistry for measles virus associated proteins. Meningitis may be caused by bacteria, mycobacteria, viruses, fungi, and parasites. Bacterial meningitis is characterized in its acute stage by abundant neutrophils within the subarachnoid space, and subpial reactive gliosis. In the chronic stage, neutrophils are supplanted by mononuclear cells, and granulation tissue and fibrosis may appeal. Tuberculous meningitis can mimic bacterial meningitis, but more commonly exhibits a patchy granulomatous infiltrate of epithelioid histiocytes, multinucleated giant cells, and mononuclear cells. Viral meningitis often shows meningeal and perivascular lymphocytic infiltrates that may extend into Virchow-Robin spaces. Because these infiltrates can be minimal and patchy, absence of inflammation on biopsy does not rule out the diagnosis. Identification of microglial nodules in the parenchyma supports an additional diagnosis of viral encephalitis. Fungal meningitis provokes a mononuclear/granulomatous inflammatory response similar to that of tuberculous meningitis, but the organisms are usually easily identified by histochemical stains. In contrast to yeast forms (Histoplasma, Blastomyces, Cryptococcus), pseudohyphal and hypha! Viral encephalitis is recognized histologically by the presence of meningeal and perivascular lymphocytes accompanied by parenchymal microglial nodules. Occasionally, a microglial nodule may be observed around a dying neuron (termed neuronophagia). Hundreds of viruses can cause encephalitis, and most do so without forming distinctive inclusions, so serologidlaboratory tests and clinical observations are usually required for diagnosis. Nevertheless, a small subset of pathogens is responsible for most clinically significant cases. This arbovirus (arthropod-borne) infection has a peak incidence in the summer or early autumn. In the chronic phase, microglial nodules are most abundant in the spinal cord, thalamus, and substantia nigra pars compacta. Herpes encephalitis is the most common cause of sporadic viral encephalitis is the United States. Asymmetric, bilateral involvement of the temporal lobes is characteristic, and when severe involves hemorrhage and necrosis. Clinically, involvement of the temporal lobes may cause hallucinations, agitation, personality changes, and psychosis. Histologically, in addition to perivascular lymphocytes and microglial nodules, biopsy material may show areas of necrosis with foamy macrophages and hemorrhage. The histopathology features widespread, robust microglial nodules with associated lymphocytes, reactive astrocytes, and occasional multinucleated giant cells that harbor the virus. Rocky Mountain spotted fever is caused by rickettsia, but can mimic viral encephalitis and is therefore mentioned here. The organism targets vascular endothelium and smooth muscle cells, and thus produces vasculitis, thrombosis, microinfarcts, and petechial hemorrhage without fibrinoid necrosis. Microglial nodules and mononuclear infiltrates with a leptomeningeal and perivascular distribution are commonly seen. Each cyst contains a scolex that can be detected radiographically or histologically and serves as the pathognomonic feature of the lesion. Death of the organism triggers a brisk mixed and granulomatous inflammatory response. Over months to years, inflammation subsides; the cyst becomes fibrotic and, eventually, a small calcified nodule.
Eosinophilic metaplasia is the designation for benign epithelium with large supranuclear eosinophilic granules women's health center edmond ok generic raloxifene 60mg otc, which represent exocrine differentiation with lysosome-like granules women's health center kirkland wa order 60mg raloxifene overnight delivery. This uncommon and typically focal change is more often seen in prostatic ductal epithelium and is associated with variable degrees of chronic inflammation and atrophy women's health clinic fillmore buy raloxifene 60 mg without a prescription. Paneth cell-like alteration may be found in nonneoplastic prostatic epithelium after radiation pregnancy vomiting 60 mg raloxifene with mastercard. Grossly, the nodules, which characteristically arise in the transition zone and periurethral area, are multiple and vary from solid white to spongy with cystic change. Mixed epithelial and stromal hyperplasia is most common, with variable admixtures of spindled stromal cells and complex benign glands with complex papillary and branching architecture (e-Fig. Microscopically, there are two or more layers of basal cells arranged in acinat; cribriform, and solid growth patterns (e-Fig. In usual basal cell hyperplasia, the basal cells are uniform and cytologically bland, whereas in so-called atypical basal cell hyperplasia prominent nucleoli are discerned. The term "atypical" should be avoided because no form of basal cell hyperplasia is a known risk factor for neoplasia. The luminal lining cells are cytologically bland and there is a prominent rim of basal cells. Mesonephric remnant hyperplasia is a very rare prostatic proliferation displaying a vaguely lobular or infiltrative pattern of small tubules with cuboidal epithelium and intraluminal, eosinophilic secretions (Am] Surg Pathol. Verumontanum gland hyperplasia is a benign, small gland proliferation of the verumontanum and adjacent posterior urethra (e-Fig. The closely packed glands can architecturally be alarming, but the lack of nuclear atypia and the presence of basal cells rules out carcinoma. Atypical adenomatous hyperplasia (adenosis) is a nodular proliferation of closely packed small acini (e-Fig. The densely packed small pale acini are sometimes intermingled with larger, more complex glands. The basal cell layer is fragmented, and, on average, 50% of glands completely lack basal cells. Adenosis can be mistaken for well-differentiated Gleason score 2 to 4 adenocarcinoma. It is found in the vast majority of radical prostatectomy specimens with prostatic carcinoma. If there is significant concern for malignancy, a diagnosis of focal glandular atypia, suspicious for carcinoma may be rendered. A diagnosis of atypia is applied in about 3% (range 1% to 9%) of needle biopsies(] Urol. Prostate cancer, which is acinar adenocarcinoma in the vast majority of cases, is a common malignancy in North America, Europe, and Australia, whereas it is less common in Asia. Prostatic adenocarcinoma is uncommonly diagnosed clinically before the age of 50, whereas a significant minority of men (around 31 %) in their 30s and 40s have a small adenocarcinoma detectable at autopsy (In Vivo. Hereditary prostatic adenocarcinoma accounts for about 10% of prostatic adenocarcinomas. Several candidate genes involved in hereditary transmission have been identified (Mod Pathol. Probable risk factors include dietary fat and androgens; potential risk factors are cadmium, low vitamin D, low vitamin E, low selenium, herbicides, and sedentary lifestyle. Thus, histopathologic tissue diagnosis is the standard to establish a diagnosis of malignancy in the prostate. Prostatic carcinoma generally does not cause symptoms until late in the course of the disease. Local growth into the urethra and bladder neck can cause increase in frequency and difficulty in urination. Metastatic spread to bone can produce pain in the lower back, chest, hip, legs, and shoulders. Acinar adenocarcinoma of the prostate is by far the most common type of prostate cancer. When visible, the carcinoma can appear nodular and white to irregular and gray or white-yellow (e-Fig. Microscopic diagnosis is based on a synthesis of a constellation of histologic attributes (Table 29. Major criteria are architecture (pattern of growth), absence of basal cells, and nuclear atypia. The architectural patterns of cellular arrangement are well depicted in the Gleason grading diagram. Well-differentiated prostatic adenocarcinoma of Gleason patterns 1 and 2 displays abnormal glandular arrangements in the form of well-circumscribed nodules of closely packed small acini (e-Fig. Gleason pattern 3 usually presents as single, small, infiltrating glands, with wide stromal separation (e-Fig. High-grade Gleason pattern 5 is composed of sheets, cords, single cells, or comedocarcinoma (e-Fig. Atrophic pattern adenocarcinoma displays decreased cytoplasm and can thereby mimic benign atrophy (e-Fig. Such cytoplasmic volume loss can be seen with or without a history of hormonal or radiation therapy.
Essential thrombocythemia is a clonal neoplasm derived from a pluripotential hematopoietic stem cell in which the majority of clinical and pathologic features are related to morphologically and physiologically abnormal megakaryocytes and platelets (Haematologica womens health of blairsville buy discount raloxifene 60mg line. There is usually a marked peripheral thrombocytosis menstruation vomiting 60 mg raloxifene for sale, generally in excess of 1 5 menstrual cycles in 2 months order raloxifene no prescription,000 x 109/L women's health issues in developing countries cheap 60 mg raloxifene visa, although a sustained count of >450 x 109/Lis sufficient for diagnosis. The platelets are frequently morphologically abnormal, including forms with decreased granularity. The most prominent characteristic of the bone marrow is marked megakaryocytic hyperplasia. The megakaryocytes are frequently morphologically abnormal, with large overall size and hyperlobate (staghorn) nuclei. A definite diagnosis can be established after other myeloproliferative neoplasms are eliminated from consideration with ancillary studies. The major pathophysiologic consequences of the thrombocytosis and proliferation of megakaryocytes are episodic bleeding and thrombosis, which are major causes of morbidity and mortality. Primary myelofibrosis (chronic idiopathic myelofibrosis, agnogenic myeloid metaplasia, myelofibrosis with myeloid metaplasia) is another myeloproliferative neoplasm attributed to transformation of a pluripotential hematopoietic stem cell. Classically, there are two phases in the natural history of disease (Hematol Oncol Clin North Am. The first phase, referred to as the cellular phase, is characterized by a marked expansion of all hematopoietic lineages; it is followed by the spent phase, characterized by progressive bone marrow failure and fibrosis. Because the cellular phase is often clinically silent, the majority of clinical findings are related to increasing bone marrow fibrosis, and include fatigue (due to anemia), bleeding (due to thrombocytopenia), and infection (due to granulocytopenia). Hepatosplenomegaly due to extramedullary hematopoiesis is a common physical finding. The cellular phase is often characterized by peripheral granulocytic leukocytosis and/or thrombocytosis. The former is sometimes accompanied by eosinophilia or basophilia clinically mimicking chronic myelogenous leukemia. In the cellular phase, the bone marrow is hypercellular due to a panhyperplasia of all hematopoietic lineages. Megakaryocytes cluster in the bone marrow and are characteristically highly atypical including large forms with bulbous/hyperchromatic nuclei. There are two important exceptions to the requirement of at least 20% blasts in acute myeloid leukemia. The second exception involves acute erythroid leukemia, for which blasts comprise at least 20% of the nonerythroid cell population, rather than at least 20% of all cells; because another requirement for acute erythroid leukemia is that at least 50% of all cells are erythroid precursors, cases with very high erythroid percentages may qualify as acute leukemia even in the presence of a very modest blast percentage. Acute leukemias, particularly in children and the elderly, may present with isolated anemia and a lack of circulating blasts. Diagnosis requires detection of at least 20% blasts in the bone marrow and/or the presence of an acute myeloid leukemia-specific cytogenetic abnormality. Although replacement of the bone marrow by fibrosis, carcinoma, sarcoma, or other nonhematopoietic cell may result in anemia, it is generally accompanied by leukopenia and/or thrombocytopenia reflecting indiscriminate displacement of normal marrow constituents. B-lymphoblastic leukemia is arbitrarily separated from its tissue analogue, lymphoblastic lymphoma, by the presence of a tissue mass and:::;20% bone marrow blasts in the latter (e-Fig. B-lymphoblastic leukemia is most common in children <6 years old; patients with purely lymphomatous disease are somewhat younger on average. In the pediatric population, cytogenetic and molecular genetic findings are highly predictive of disease outcome. Predictors of poor outcome include the following: age <4 years or > 10 years, hypodiploidy, t(9;22)(q34;q11. A special category of lymphoblastic leukemia is the leukemic analogue of Burkitt lymphoma. Patients with this disease commonly present with an abdominal mass (Western Europe and North America) or a jaw lesion (Africa). T-lymphoblastic leukemia/lymphoma is less common and involves an older demographic than its B-cell counterpart. Patients typically present with abundant blasts in the peripheral blood and a mediastinal mass. Although T-lymphoblastic malignancies have historically had a poor prognosis, recent innovations in treatment have improved outcome. For most non-Hodgkin lymphomas, diagnosis is made following biopsy of an involved lymph node or extramedullary focus of disease, and bone marrow biopsy is performed for staging rather than precise classification. Because B-celllymphomas are more common than T-cell tumors, the former are better characterized. Marginal zone lymphomas may demonstrate follicular colonization when they occur in bone marrows with lymphoid aggregates. Overall, the likelihood of marrow involvement by non-Hodgkin lymphoma is highly variable depending on type, ranging from very common. Immunohistochemistry is typically not required in non-Hodgkin lymphoma staging biopsies, although it is occasionally helpful in delineating benign from malignant lymphoid aggregates. Most commonly, the affected individual is a middle-aged man presenting with pancytopenia, including lymphopenia and monocytopenia, and an enlarged spleen. Although identified in bone marrow aspirate preparations, hairy cells are more easily identified in the peripheral blood by the presence of cytoplasmic projections (hence the name "hairy cell leukemia," e-Fig. The malignant cells frequently have an interstitial pattern of involvement of the bone marrow and for this reason are occasionally overlooked.
Lasers illuminate the particles in the sample stream and optical mirrors and filters route the different wavelengths of the generated light scatter and fluorescent signals to the appropriate photodetectors women's health vitamins and minerals generic raloxifene 60 mg with visa. For example menopause 1 ovary discount raloxifene online master card, lymphocytes will show both a low forward scatter and a low side scatter due to the small size and lack of cytoplasmic granulation women's health controversial issues generic raloxifene 60mg visa. In contrast breast cancer0rg buy generic raloxifene 60mg on line, neutrophils are larger in size and show granular cytoplasm as well as a complex nucleus, and therefore will show both a high forward and a side scatter (e-Fig. Another way to identify particular subpopulations is to conjugate fluorescent dyes to monoclonal antibodies directed toward antigens on a particular cell subset. The staining procedure can be carried out in a direct or indirect staining process. The direct staining procedure involves a single staining incubation, followed by several washes to remove nonspecifically bound antibodies. The indirect staining procedure involves the incubation of cells with a nonfluorescent monoclonal antibody directed toward the specific antigen. After washing to remove nonspecifically bound antibody, there is a second incubation with a fluorescent antibody directed against the monoclonal antibody. The optical system consists of lasers to illuminate the cells in the sample stream and optical filters to direct the resulting light signals to the appropriate dete<:tors. The electronic system converts light signals into electronic signals that are processed by the computer. Amplification of a signal detected by a photodetector can be achieved by means of log amplification or linear amplification. Log amplifiers are usually used to separate negative from dim positive signals, and are commonly used for signals from cells stained with fluorochrome-labeled antibodies because these cells often exhibit a great range of fluorescence intensities. An electronic threshold is used to limit the number of events to the population of interest. Aher the acquired data are saved, the cell populations can be displayed by several different types of data plots. Flow cytometry has become a valuable ancillary method for classifying acute leukemias and lymphomas. Monoclonal antibody technology has provided flow cytometry with a large variety of antibodies specific to nuclear, cytoplasmic, and surface antigens characteristic of particular cell subsets. Flow cytometric scattergrams of an example of precursor B-lymphoblastic leukemia are shown in e-Figure 57. The three significant milestones in the history of clinical cytogenetics are the preparation of chromosome spreads from peripheral blood cultures (Exp Cell Res. The remarkable advancement of the field of human cytogenetics is emphasized by the fact that it has been only 50 years since the correct number of human chromosomes was established. The various banding methods in current use not only permit identification of each chromosome, but also make it possible to detect specific alterations associated with hereditary syndromes and neoplasms. The utility of the technique in surgical pathology rests on the fact that specific cytogenetic abnormalities have been recognized that are closely, and sometimes uniquely, associated with morphologically and clinically distinct subsets of lymphoma and leukemia, or with soft tissue neoplasms. Cancer cytogenetic studies have greatly aided targeted therapy, prognosis, and risk-based stratification of intensity of therapy. The power of conventional cytogenetics lies in its ability to provide simultaneous analysis of the entire genome without any foreknowledge of the chromosomal regions involved in the disease process. In most cases, the type and location of an identified chromosomal abnormality is either directly diagnostic or can be used to direct additional testing. The clinical utility of traditional cytogenetic analysis is restricted by two general features of the method. From a technical standpoint, analysis can only be performed on viable tissue specimens that contain proliferating cells (discussed in more detail below). From a sensitivity standpoint, analysis has resolution of only about 3 to 4Mb at an 850-band level, and only about 7 to 8 Mb at a 400-band level. Traditional cytogenetic analysis is therefore only suited for detection of numerical abnormalities and gross structural rearrangements. The method does not have the sensitivity to detect mutations such as small deletions and amplifications, single base pair substitutions, and so on. Chromosomes that can be individually distinguished by light microscopy can only be obtained during cell division, and so the fundamental requirement for traditional cytogenetic analysis is a tissue specimen that contains actively proliferating cells, or cells that can be induced to proliferate in vitro. The basic method for production of metaphase chromosomes for cytogenetic analysis is shown in Figure 58. Different specimen types have different sample and han~ dling requirements (Table 58. Inappropriate handling, as well as delay between specimen collection and culture initiation, can markedly decrease the likelihood that the sample will grow in vitro, so communication and coordination with the cytogenetics laboratory are essential. In vitro culture relies on a sterile microenvironment, and so specimens should be collected under sterile conditions. In practice, sterility is most difficult to achieve when sampling solid tissues; in this setting, clean instru~ ments and a clean cutting surface, together with transport of the specimen in medium supplemented with broad~spectrum antibiotics, can be used to minimize contamination. Bone marrow and solid tissue neoplasms consist of cell types that proliferate spontaneously in culture, although often at a low rate.
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