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The residual function and -globin production determine the severity of the anemia women's health for over 50 generic 100mg female viagra with visa. F 0 1 2 A1 A2 5 6 0 3 4 Time in minutes Figure 4-17 -Thalassemia major womens health 3 week workout plan order female viagra 50 mg otc, gross Severe menstrual hygiene day buy female viagra 100 mg with mastercard, chronic anemias menstruation thesaurus purchase female viagra 50 mg fast delivery. This drive for erythropoiesis may increase the mass of marrow and lead to an increase in marrow in places, such as the skull seen here, where it is not normally found. Such an increase in marrow in skull may lead to "frontal bossing" or forehead prominence because of the skull shape change. The result can be bony prominence with prominent epiphyseal regions, as seen in this 20-year-old man. The hemochromatosis can lead to dilated cardiomyopathy, hepatic failure, hypogonadism, and "bronze" diabetes mellitus from iron deposition in islets of Langerhans. Figure 4-19 -Thalassemia major, microscopic -Thalassemia major can lead to a severely hydropic stillborn fetus. Embryonic hemoglobins and are present here, but they do not persist after birth and cannot compensate. The tetramer of chains forms Hgb H, which may be seen in small amounts in neonates with -Thalassemia minor. Larger amounts (10% to 25%) of Hgb H persist in persons with three abnormal -globin chains (Hgb H disease). Anisocytosis (variation in size) and poikilocytosis (variation in shape) are also increased. Iron deficiency anemia is common, and individuals at greatest risk are children and women in their reproductive years (from menstrual blood loss and from pregnancy). This suggests a toxic injury to the bone marrow, such as lead poisoning or drug effect. Such stippling may also appear with severe anemia, such as a megaloblastic anemia or thalassemia. The most common cause is drugs known to be toxic to bone marrow, such as chemotherapy agents. Exposure to a drug such as a sulfonamide or to toxic substances such as benzene may precede development of an aplastic marrow. These agents may damage or suppress stem cells from which the erythroid, myeloid, and megakaryocytic cells are derived. Figure 4-25 Myelophthisic anemia, microscopic the marrow spaces between the reactive woven bone are filled with metastatic carcinoma replacing normal hematopoietic cells. A space-occupying process that destroys substantial marrow and reduces hematopoiesis is known as a myelophthisic process. Metastases, leukemias, lymphomas, and extensive infections can produce this effect. Multiple cultures and special stains are done to find an infectious cause, such as a mycobacterial or fungal infection. In this case, no organism was shown, and the clinical features fit with sarcoidosis. Figure 4-28 Myelofibrosis with teardrop cells, microscopic this peripheral blood smear shows teardrop cells. There is reticulin fibrosis filling the marrow spaces, reduction in hematopoiesis, and peripheral pancytopenia. A reticulocyte is present here, but the reticulocyte count would not be as increased as it should be, given that the marrow reserve is gone. Figure 4-29 Malaria, microscopic Malaria is a parasitic disease of erythrocytes caused by the parasitic genus Plasmodium, of which the following species affect humans: Plasmodium vivax, Plasmodium falciparum, Plasmodium ovale, Plasmodium knowlesi, and Plasmodium malariae. After transmission via the Anopheles mosquito, initial replication occurs in the liver, followed by the erythrocytic phase producing recurrent fever with hemolysis and anemia. This organism produces the clinical picture of "relapsing fever" and is spread by lice and ticks. Variable expression of surface proteins helps these organisms evade immune destruction. Antibiotic therapy, especially with penicillin, can induce extensive cytokine release (Jarisch-Herxheimer reaction) with pronounced febrile reaction. Figure 4-31 Leishmaniasis, microscopic A myelophthisic anemia may result from infections involving the marrow, including fungal, mycobacterial, and parasitic infections. Seen here are multiple amastigotes of Leishmania donovani infantum in a bone marrow smear. The infiltrative process does not have to fill up much of the marrow to produce a characteristic peripheral blood leukoerythroblastic pattern. The visceral form of this disease, also involving liver and spleen, can cause fever, weight loss, hepatosplenomegaly, and pancytopenia. Figure 4-32 Babesiosis, microscopic Babesiosis caused by infection with Babesia microti is a rare tick-borne disease endemic to the northeastern United States and parts of Europe. Infective larvae transmitted by mosquito bite migrate either to lymphatics (Wuchereria bancrofti, Brugia malayi) or to subcutaneous connective tissues (Onchocerca volvulus). In lymphatic filariasis, the worms cause lymphedema of lower extremities, external genitalia, and sometimes upper extremities, called elephantiasis because of marked enlargement. Onchocerciasis can cause blindness, dermatitis with pruritus, depigmentation or hyperpigmentation, and fibrosis with nodularity. The bite of the tsetse fly introduces infective trypomastigotes into the circulation, where they divide and multiply and spread to lymph nodes and spleen.

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A thin connective tissue layer breast cancer x-ray discount female viagra 50mg fast delivery, the endoneurium women's health center weirton wv discount female viagra line, surrounds individual nerve fibers women's health clinic gateshead buy discount female viagra on-line. Most sensory fibers are unmyelinated menstruation every two weeks buy discount female viagra online, although fibers for fine discriminatory senses, such as touch and vibration, are myelinated. The major component of an axonal myelin sheath is myelin protein zero, and myelin basic protein is the second most common structural protein. Figure 18-2 Normal peripheral nerve, microscopic this normal peripheral nerve in transverse section with toluidine blue stain in the left panel has blue-black myelin around a normal number and distribution of thickly and thinly myelinated fibers. Myelinated fibers transmit impulses with higher conduction velocity (6 to 120 m/sec) than nonmyelinated fibers (0. Note the even spacing between the dark myelin lamellae around an axon in the electron micrograph in the right panel. Figure 18-3 Normal peripheral ganglion, microscopic this peripheral ganglion has nerve cell bodies and surrounding satellite cells and interstitial fibroblasts. The nerve cell bodies have fine pink Nissl granules, and some nerve cells display light-brown lipochrome pigment within their cytoplasm. The sensory and the postganglionic autonomic nerve fibers have neuronal cell bodies located in ganglia associated with cranial nerves, dorsal spinal roots, and autonomic nerves. Each fiber is bounded by a sarcolemma, which projects into the cytoplasm as T tubules containing a high concentration of calcium ions. A nerve impulse causes depolarization with release of the calcium ions to initiate muscle contraction. Figure 18-5 Normal skeletal muscle, microscopic In longitudinal section, a skeletal muscle fiber has prominent cross-striations formed by the Z discs. The thin actin filaments are attached to Z discs and interdigitate with the thick myosin filaments to allow muscle contraction. The additional proteins tropomyosin and troponin complex regulate actin, myosin, and calcium binding. The skeletal muscle fiber is a multinucleated cell with numerous sarcolemmal nuclei at the periphery of each muscle fiber. Occasional satellite cells provide for maintenance, repair, and regeneration of injured fibers. Type I fibers have more mitochondria and more myoglobin for sustained contraction. The motor units are small in number (<50 myofibers) when fine motor control is required (extraocular muscles) and large (hundreds of myofibers) in postural muscles, such as the quadriceps femoris. In this distal nerve segment in longitudinal section, small axonal and myelin fragments lie within myelin ovoids as vacuolar digestion chambers. Regeneration may be possible because the proximal nerve stump undergoes axonal sprouting, and Schwann cells proliferate to remyelinate the nerve fiber. Regeneration proceeds along the course of the degenerated axon at a rate of about 2 mm/day. Figure 18-8 Peripheral nerve with axonal sprouting, microscopic Here is axonal regrowth in a plastic-embedded cross-section of a peripheral nerve after transection, with clusters of regrowing axons surrounded by the basement membrane of a Schwann cell. Such small clusters of thinly myelinated fibers represent regrowth (axonal sprouting). Figure 18-9 Denervation atrophy, microscopic this modified Gomori trichrome stain shows the neurogenic form of skeletal muscle atrophy, with the characteristic pattern of "grouped atrophy" of muscle fibers that have lost their innervation from a lower motor neuron. These affected muscle fibers do not die, but downsize with loss of actin and myosin, becoming small and angular. There is an acute ascending paralysis that occurs over days, advancing distally to proximally. A bacterial (Campylobacter jejuni) or viral (cytomegalovirus) illness may precede the onset of this disease. Figure 18-11 Demyelination, electron microscopy this peripheral nerve shows a demyelinated axon next to an internode. During recovery from this form of inflammatory neuropathy, these areas become remyelinated. Examination of the cerebrospinal fluid shows few inflammatory cells, little or no pleocytosis, but an elevated protein. Figure 18-12 Chronic inflammatory demyelinating polyneuropathy, microscopic In this sural nerve biopsy specimen on crosssection note the "onion bulb" formation from excessive proliferation of Schwann cells after recurrent demyelination and remyelination from macrophage response to immunoglobulin deposition. This is the most common chronic acquired inflammatory peripheral neuropathy, lasting from months to years, usually with relapses and remissions. End glycosylation of proteins and sorbitol accumulation in cells not requiring insulin for glucose uptake can underlie the pathogenesis of this neuropathy, driven by hyperglycemia. Figure 18-14 Hansen disease, microscopic A poorly formed granuloma appears around a peripheral nerve within the dermis. The leprosy bacilli (Mycobacterium leprae) grow best just below body temperature, preferring the cooler skin and peripheral nerves. Hypopigmented patches or macular lesions with decreased sensation develop on the face, extremities, and trunk. Nodular disfiguring lesions can appear, with the lepromatous form having many macrophages filled with numerous acid-fast bacilli (globi). Shown here is the borderline form, with some organisms and some epithelioid cells.

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Figure 10-39 Membranous nephropathy pregnancy glucose test female viagra 50 mg lowest price, microscopic A Jones silver stain of this glomerulus highlights the proteinaceous basement membranes of capillary loops in black menopause gas bloating order female viagra line. There are characteristic "spikes" involving the capillary loops with membranous nephropathy women's health issues news buy female viagra with paypal, shown here with black basement membrane material appearing as small projections distributed within the capillary loops breast cancer backgrounds purchase female viagra now. The immune complexes, not highlighted by the Jones stain, lie between the black spikes. Loss of anticoagulant proteins in nephrosis predisposes to thrombosis, including renal vein thrombosis. Urinalysis with nephrotic syndrome may show lipiduria and proteinuria, whereas blood lipids (cholesterol and triglyceride) are increased. Figure 10-40 Membranous nephropathy, electron microscopy the immunofluorescence pattern here has a "bumpy" or granular staining pattern as a result of irregular deposition of immune complexes within the basement membranes of the glomerular capillary loops. Various fluorescein-labeled antibodies can be employed, such as those directed against immunoglobulins or complement components, which commonly compose the immune complexes. The onset of membranous nephropathy is often gradual, with nephrotic syndrome a likely presenting finding. The "spikes" seen with the silver stain are the lighter areas representing the intervening increased matrix of basement membrane between the darker immune deposits. These deposits invariably contain complement proteins, and the C5b-C9 membrane attack complex damages glomerular capillaries. The loss of basement membrane function leads to proteinuria, which is often "selective" because mostly lower molecular weight proteins such as albumin are lost. Some cases have nonselective proteinuria with hematuria, and up to 40% of cases may eventually progress to chronic renal failure. Normal fenestrated endothelium is present, and the basement membranes are normal in thickness with no immune deposits. Overlying epithelial cell (podocyte) foot processes are effaced (giving the appearance of fusion) and run together, which leads to loss of the normal anionic charge barrier such that albumin selectively leaks out, and proteinuria ensues, often with nephrotic syndrome. Only 3 of 10 glomeruli in the entire biopsy specimen were involved, a focal process. This disease is focal, involving some glomeruli, and segmental, involving part of the glomerulus. Both proteins are components of the slit diaphragm between podocyte foot processes. Figure 10-45 Membranoproliferative glomerulonephritis, microscopic this glomerulus has increased overall cellularity, mainly mesangial. On light microscopy there is mesangial proliferation, increased mesangial matrix, mesangial immune complex deposition, accentuation of the lobular architecture, and increased leukocytes. Most cases occur in adolescents and young adults, with both nephrotic and nephritic features. The dense deposits within the basement membrane often coalesce to form a ribbonlike mass of deposits. The deposits result from activation of the alternative complement pathway, evidenced by a reduced serum C3 with normal C1 and C4. Patients with dense deposit disease often have circulating C3 nephritogenic factor (C3NeF). The rare condition, called partial lipodystrophy with C3NeF activity, may be accompanied by dense deposit disease. Figure 10-49 IgA nephropathy, microscopic In IgA nephropathy, there is abnormally glycosylated IgA1. Antiglycan antibodies form and lead to immune complexes deposited within the mesangium of the glomeruli. Some viruses and bacteria express N-acetylgalactosamine on their cell surfaces so that infection may promote antiglycan antibody formation; IgA nephropathy may initially appear in association with an upper respiratory or gastrointestinal infection. This disease most often tends to be mild, but recurrent, and continues with normal renal function for years. Some cases are associated with celiac disease and some with chronic liver disease from decreased IgA clearance. In general, greater immune complex deposition and more cellular proliferation suggest a worse prognosis. In this case there is extensive immune complex deposition in the thickened glomerular capillary loops, giving a wire-loop appearance. Figure 10-52 Alport syndrome, microscopic this disease is a form of hereditary nephritis accompanied by nerve deafness and eye problems, such as lens dislocation, cataracts, and corneal dystrophy. Although onset of microscopic hematuria or proteinuria occurs in childhood, renal failure is more likely to occur in adults. The renal tubular cells appear foamy because of the accumulation of neutral fats and mucopolysaccharides, seen here imparting a pale red appearance with a fat stain. In contrast, renal diseases that are "nephrotic" are characterized by the presence of protein spilled into the urine. Steadily increasing serum creatinine and urea nitrogen are clues to this progression. The cortex is fibrotic, the glomeruli are sclerotic from hyaline obliteration, there are scattered interstitial chronic inflammatory cell infiltrates, and the arteries are thickened. Tubules are often dilated and filled with pink casts and give an appearance of "thyroidization. Diminished renal clearance of phosphate predisposes to secondary hyperparathyroidism.

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Superior and anterior movement of s ternum Innervation the diaphragm is innervated by the phrenic nerves (C3 menopause memory problems order female viagra with paypal, C4 menstrual blood smell generic 50 mg female viagra visa, and C5) women's health clinic philadelphia order 50mg female viagra, which penetrate the diaphragm and innervate it from its abdominal surface womens health yahoo purchase female viagra 100mg mastercard. Contraction of the domes of the diaphragm attens the diaphragm, increasing thoracic volume. Elevation and depression of the diaphragm signi cantly alter the vertical dimensions of the thorax. Changes in the anteroposterior and lateral dimensions result from elevation and depression of the ribs. The posterior ends of the ribs articulate with the vertebral column, whereas the anterior ends of most ribs articulate with the sternum or adjacent ribs. Because the anterior ends of the ribs are inferior to the posterior ends, when the ribs are elevated, they move the sternum upward and forward. Also, the angle between the body of the sternum and the manubrium may become slightly less acute. This "pump handle" movement changes the dimensions of the thorax in the anteroposterior direction. As well as the anterior ends of the ribs being lower than the posterior ends, the middle of the shafts tend to be lower than the two ends. This "bucket handle" movement increases the lateral dimensions of the thorax. Pleura Each pleural cavity is lined by a single layer of at cells, mesothelium, and an associated layer of supporting connective tissue; together, they form the pleura. The pleura is divided into two major types, based on location: pleura associated with the walls of a pleural cavity is parietal pleura. Parietal pleura Vis ceral pleura Clinical app the arrangement of pleural cavities is clinically signi cant the pleural cavities are completely separated from each other by the mediastinum. Therefore, abnormal events in one pleural cavity do not necessarily affect the other cavity. This also means that the mediastinum can be entered surgically without opening the pleural cavities. Another important feature of the pleural cavities is that they extend above the level of rib I. As a consequence, abnormal events in the root of the neck can involve the adjacent pleura and lung, and events in the adjacent pleura and lung can involve the root of the neck. Medias tinum Left pleural cavity Cos todiap hragmatic reces s Diaphragm Right pleural cavity 78. This sleevelike covering, and the structures it contains, forms the root of the lung. The root joins the medial surface of the lung at an area referred to as the hilum of lung. The costal pleura is innervated by branches from the intercostal nerves and pain would be felt in relation to the thoracic wall. The diaphragmatic pleura and the mediastinal pleura are innervated mainly by the phrenic nerves (originating at spinal cord levels C3, C4, and C5). Pain from these areas would refer to the C3, C4, and C5 dermatomes (lateral neck and the supraclavicular region of the shoulder). The visceral pleural is innervated by visceral afferent bers that accompany bronchial vessels and pain is generally not elicited from this tissue. Each pleural cavity is the potential space enclosed between the visceral and parietal pleurae. As a result, the surface of the lung, which is covered by visceral pleura, directly opposes and freely slides over the parietal pleura attached to the wall. The peripheral re ections of parietal pleura mark the extent of the pleural cavities. Superiorly, the pleural cavity can project as much as 3 to 4 cm above the rst costal cartilage, but does not extend Peripheral re ections Midc lavic ular line Midaxillary Parietal pleura the names given to the parietal pleura correspond to the parts of the wall with which they are associated. The dome-shaped layer of parietal pleura lining the cervical extension of the pleural cavity is cervical pleura (dome of pleura or pleural cupola). Covering the superior surface of the cervical pleura is a distinct domelike layer of fascia, the suprapleural membrane. Superiorly, the membrane receives muscle bers from some of the deep muscles in the neck (scalene muscles) that function to keep the membrane taught. The suprapleural membrane provides apical support for the pleural cavity in the root of the neck. This limitation is caused by the inferior slope of rib I to its articulation with the manubrium. Anteriorly, the pleural cavities approach each other posterior to the upper part of the sternum. However, posterior to the lower part of the sternum, the parietal pleura does not come as close to the midline on the left side as it does on the right because the middle mediastinum, containing the pericardium and heart, bulges to the left. The largest and clinically most important recesses are the costodiaphragmatic recesses, which occur in each pleural cavity between the costal pleura and diaphragmatic pleura. The costodiaphragmatic recesses are the regions between the inferior margin of the lungs and inferior margin of the pleural cavities. During expiration, the inferior margin of the lung rises and the costodiaphragmatic recess becomes larger. Costodiaphragmatic recesses Visceral pleura the visceral pleura is continuous with the parietal pleura at the hilum of each lung where structures enter and leave the organ. The visceral pleura is rmly attached to the surface of the lung, including both opposed surfaces of the ssures that divide the lungs into lobes. Clinical app Pleural recesses the lungs do not completely ll the anterior or posterior inferior regions of the pleural cavities. Expansion of the lungs into these spaces usually occurs only during forced inspiration; the recesses also provide potential spaces in which uids can collect and from which uids can be aspirated.