Denise M. Fitzpatrick, RNC, MSN, CNE

• Course Coordinator
• Abington Memorial Hospital, Dixon
• School of Nursing
• Willow Grove, Pennsylvania

Patients present with multiple bilateral nodules that tend to be peripheral in location and well defined chronic gastritis gerd best order for ranitidine. A vessel may be identified coursing directly into the center of a nodule gastritis or morning sickness buy ranitidine 150 mg overnight delivery, termed the "feeding vessel sign gastritis diet ������� buy discount ranitidine 150 mg on-line," thought to represent the hematogenous source of the nodule gastritis diet 9 month cheap 150 mg ranitidine with mastercard. However gastritis diet ideas 300mg ranitidine free shipping, this sign is not specific for septic emboli gastritis diet quizzes purchase ranitidine 150mg, as it may also be seen in metastatic disease. Pulmonary manifestations include multiple lung nodules that may range from 2 to 10 cm. Of particular note is the tendency to disappear with successful therapy as subcutaneous rheumatoid nodules heal. Diagnosis Metastatic disease P Pearls y Because of blood flow, hematogenous spread (whether of infection or neoplasm) tends to favor the lower lobes. Reactivation disease presents clinically with night sweats, fever, and weight loss. Radiographically, this phase manifests as multiple cavitations reflecting the increased inflammation and necrosis. These are predominantly in the upper lobes where the higher oxygen tension enables the aerobic bacterium to thrive and where lymphatic clearance is less than that of the lower lobes. Coccidioidomycosis is a soil-borne fungus that is endemic to the Southwestern United States and is spread by inhalation. It is typically located centrally with involvement of hilar or mediastinal lymph nodes. Additional Differential Diagnoses y Pyogenic infection (pulmonary abscess, septic emboli). Staphylococcus aureus is the most common bacterial infection to result in cavitation. It typically causes a widespread consolidation and may lead to cavitation and abscess formation. In the setting of multiple widespread cavities, a source of showering septic emboli should be considered. The most common pulmonary manifestations are multiple lung nodules, followed by air-space consolidations, groundglass opacities, and thick-walled cavitations. Pulmonary infection with Mycobacterium tuberculosis is classified as primary or reactivation based on clinical and radiographic features. Predominantly, a lower lobe air-space disease, mediastinal lymphadenopathy, and pleural effusions are typical radiographic manifestations of primary infection. Fungal infection in the lung encompasses both primary infection in immunocompetent patients. Histoplasma, Coccidioides,blastomycosis) and opportunistic infection in immunosuppressed patients. The pneumoconioses result from inhalation of particulate matter as a result of occupational exposure. Radiographic findings consist of multiple upper lobe fibrotic nodules ranging from 1 to 10 mm in size. A late complication referred to as progressive massive fibrosis presents radiographically as upper lobe masslike opacities in the setting of underlying fibrosis. Acute varicella pneumonia is a severe form of primary infection which occurs primarily in children and pregnant patients. The infection presents as multifocal regions of patchy air-space disease, and affected patients are very ill. Healed varicella presents radiographically as calcified miliary pulmonary nodules in a random distribution. Following exposure, the acute phase may exhibit fine nodular or groundglass opacities. Centrilobular nodules with ground-glass opacities are typical of the subacute phase of the disease, most often in the mid- to lower lung zones. If exposure continues, there may be progression to end-stage lung disease with fibrosis. Metastatic spread of tumors within the chest may take a variety of routes including direct, hematogenous, lymphatic, and endobronchial spread. While hematogenous spread is the most common form of widespread dissemination, endobronchial spread is also possible in late stages of disease and may manifest as centrilobular nodules in any part of the lung. Either perilymphatic or centrilobular nodules may be present, which may eventually coalesce to form masslike opacities and potentially calcify. Late findings may include masslike fibrosis with peripheral emphysema (progressive massive fibrosis). Diagnosis Hypersensitivity pneumonitis P Pearls y Mycobacteria are common causes of infectious bronchiolitis; a "tree-in-bud" appearance is characteristic. Emphysema is characterized by nonfibrotic enlargement of the airways distal to the terminal bronchioles with destruction of alveolar walls. Centrilobular emphysema involves the central portion of the secondary pulmonary lobule with upper lobe predominance and is highly associated with cigarette smoking. Panlobular emphysema involves the entire lobule and is classically associated with alpha-1 antitrypsin deficiency. Paraseptal emphysema is predominantly subpleural, involving the alveolar ducts and sacs. The most common cause of diffuse pneumonia in immunocompromised patients, Pneumocystis pneumonia classically results in central ground glass opacities with or without reticulonodular interstitial thickening on plain radiographs. Diagnosis Lymphangioleiomyomatosis P Pearls y Cysts and emphysema can coexist but are distinct processes; centrilobular emphysema is most common. Plain radiographs reveal increased interstitial markings at the lung bases with normal-to-low lung volumes. Occasionally, ground-glass opacities may been seen, which correlate with regions of active alveolitis. Scleroderma is a systemic process that affects young females and involves many organ systems-the lungs, esophagus, and musculoskeletal system. Asbestos-related lung disease results from occupational exposure, as can be seen in former shipyard workers and mechanics. The clinical and radiographic manifestations usually present 20 years after the initial exposure. Pleural thickening and pleural plaques are the most common radiographic manifestation and are typically bilateral, involving predominantly the lower thorax. Rounded atelectasis is a common finding and presents as a rounded mass, which abuts the pleura in a region of underlying pleural thickening. Lung involvement can include lower lobe septal thickening and subpleural honeycombing. Other patterns of injury include pulmonary edema, pulmonary hemorrhage, and hypersensitivity pneumonitis. There are coarsened, irregular interstitial markings and countless small nodules predominantly within the upper lobes. Parenchymal involvement can range from poorly defined opacities to lobar consolidations. There is no distribution preference, and cavitation, though possible, is not common. Sarcoidosis is a systemic disease of unknown etiology characterized by noncaseating granulomas. Parenchymal involvement usually consists of countless 2- to 4-mm centrilobular and subpleural (perilymphatic) nodules. Sarcoid granulomas can resolve completely; however, they occasionally cause severe and extensive fibrosis that resembles progressive massive fibrosis that is seen in complicated silicosis. The lungs and gastrointestinal tract are most affected with thick secretions from exocrine glands. Pneumoconiosis is a broad term that describes reactions of the lungs to inhaled dust particles. Silicosis is caused by the inhalation of free silica, a compound associated with mining of heavy metal, sandblasting, and stonework. Patients may present acutely following heavy exposure whereby silicoproteinosis develops or, more commonly, with chronic silicosis from decades of exposure. The chronic form results from cyclic inflammation, resulting in fibrosis with upper lobe predominance. Complicated silicosis is an extreme progression where the fibrosis coalesces into masslike opacities, a process called progressive massive fibrosis. The hallmark of airway obstruction in children is air trapping, which is manifested as failure of the lung to decrease in volume, and subsequently increase in opacification, on expiratory chest radiographs. Air trapping occurs when an endobronchial lesion causes a check-valve type of obstruction. In children, this is usually secondary to foreign body aspiration (which may be radiolucent). Oligemia of the lung beyond the occluded pulmonary vessel, or the Westermark sign, is a helpful but not commonly encountered sign of pulmonary embolism. A large unilateral thrombus, whether bland, septic, or neoplastic, can result in a unilateral hyperlucent lung. A pneumothorax results in hyperlucency of the ipsilateral hemithorax and typically presents with central displacement of the visceral pleural line, absence of lung markings distal to the displaced pleural line, and possible contralateral shift of the mediastinum (tension pneumothorax). In a supine patient, a pneumothorax may collect anteromedially, in the nondependent portion of the thorax. This will result in the pneumothorax presenting as lucency in the anteromedial chest rather than as a pleural line. For example, mastectomy results in relative radiolucency on the side of breast tissue removal. Poland syndrome is characterized by a spectrum of abnormalities ranging from isolated absence of the pectoralis major muscle to additional abnormalities of the ipsilateral extremity, such as syndactyly, brachydactyly, and rib anomalies. The portions of the lung ventilated by abnormal airways remain inflated by collateral air drift. Chest radiographs demonstrate unilateral hyperlucency because of reduced lung perfusion. Hyperlucency in asthma is secondary to bronchoconstriction and compensatory vasoconstriction of hypoventilated portions of the lung. As this is usually a more central process, findings are commonly bilateral but may be asymmetric. Diagnosis Chest wall abnormality (Poland syndrome) P Pearls y Expiratory views, decubitus views, and fluoroscopy may be helpful in evaluating for foreign bodies. The normal thymus increases from birth to puberty, after which it begins to involute over a 5- to 15-year period. The thymus itself may be abnormally enlarged, as in thymic hyperplasia or thymic rebound, or abnormally infiltrated, as in lymphoid follicular hyperplasia. A number of masses and tumors can arise from the thymus, including thymoma, thymic carcinoma, thymic carcinoid, cysts, lipomas, and lymphoma. Thymomas (most common) most often occur in the third and fourth decades of life and may be associated with myasthenia gravis. Mediastinal masses of thyroid origin are almost always contiguous with the thyroid gland. A truly ectopic mediastinal mass without a connection to the thyroid is possible but uncommon. Calcifications may be present, but in the end, differentiation between goiter and thyroid carcinoma is difficult unless lymphadenopathy, destruction of adjacent structures. The majority are located in the anterior mediastinum and present during the second through fourth decades of life. Teratomas, which contain elements of all germinal layers, can include skin, hair, fat, and bones if well differentiated. Approaching the patient with an anterior mediastinal mass: a guide for radiologists. Lymphadenopathy is a nonspecific finding that may be reactive or neoplastic in etiology. Lymphoma is high on the differential diagnostic list, and metastasis, particularly if patient has a known primary, must be considered. The pattern and appearance of lymphatic spread in the thorax may vary depending on the causative etiology. Low-attenuation nodes may reflect necrosis in the setting of tuberculosis, fungal infection, metastasis, and lymphoma. Enhancing nodes may be seen in the setting of Castleman disease, hypervascular metastases, tuberculosis, and rarely sarcoidosis. Vascular abnormalities must always be considered initially in the differential of a middle mediastinal mass, particularly if in proximity to the aorta. Possible causes of abnormal aortic and middle mediastinal contours include thoracic aortic aneurysm, penetrating aortic ulcers, and pseudoaneurysms. Aortic aneurysms (diameter > 4 cm) can be described by their shape (fusiform or saccular) and by the extent of wall involvement (true or false aneurysm).

The cortical/subcortical tubers are composed of disorganized glial tissue and heterotopic neuronal elements gastritis youtube order generic ranitidine online. They present as triangular regions of cortical and subcortical signal abnormality which may calcify and occasionally demonstrate enhancement gastritis diet and treatment purchase cheap ranitidine on-line. Subependymal nodules have variable T1 and T2 signal intensity and commonly enhance gastritis ginger generic ranitidine 300mg otc. They demonstrate gradient echo susceptibility (hypointensity) when calcified; the majority are calcified by 20 years of age gastritis diet ������ buy ranitidine discount. Heterotopic gray matter results from arrest or disruption of normal neuronal migration from the subependymal region to the overlying cortex gastritis diet ���� cheap ranitidine 150mg on line. Toxoplasmosis also causes intracranial calcifications; however diet for chronic gastritis patients 300 mg ranitidine overnight delivery, the distribution is more random with less propensity for the periventricular region. Common associated findings include microcephaly and neuronal migration abnormalities, including polymicrogyria and pachygyria. Extracranial metastases from multiple primary sites may involve the subependymal surfaces and choroid plexus, particularly breast carcinoma. Diagnosis Tuberous sclerosis P Pearls y Tuberous sclerosis results in subependymal nodules, which calcify and demonstrate enhancement. Brain parenchyma is compressed anteriorly and superiorly with volume loss throughout, including the posterior fossa. Hydrocephalus refers to ventriculomegaly due to obstruction, overproduction, or decreased absorption. Massive hydrocephalus compresses the brain parenchyma along the peripheral calvarial margin, mimicking hydranencephaly or holoprosencephaly. Key distinguishing features include a thin mantle of cortex along the inner calvarium and the presence of the falx, respectively. Other causes include obstructing posterior fossa, pineal gland, tectal plate, and intraventricular masses. Nonobstructive communicating hydrocephalus may be seen with prior meningitis, ventriculitis, or hemorrhage. Hydranencephaly is characterized by liquefactive necrosis of the supratentorial brain parenchyma in the anterior (internal carotid artery) circulation secondary to some form of in utero insult. There is sparing of parenchyma in the posterior (posterior cerebral artery and cerebellar branch vessels) circulation. Most cases are thought to result from an ischemic, traumatic, or toxic insult between approximately 20 and 27 weeks of gestation. Neonates commonly present with neurologic function limited to the brainstem; death typically occurs in infancy or early childhood. Holoprosencephaly is a spectrum of congenital forebrain malformations characterized as alobar, semilobar, and lobar. The alobar form is the most severe and is characterized by a large dorsal interhemispheric cyst and fusion of the thalami and remaining brain parenchyma, which is flattened anteriorly. The corpus callosum, anterior falx, interhemispheric fissure, and Sylvian fissures are absent. Craniofacial abnormalities include hypotelorism, fused metopic suture, and cleft palate. Semilobar and lobar variants are less severe forms with varying degrees of defective separation of the anterior and central brain structures and complete or partial absence of the falx. The interhemispheric cysts result in lateral displacement of the brain parenchyma. The abnormality may be bilateral in up to half of cases and may be associated with septo-optic dysplasia. Patients often present with seizures and varying degrees of developmental delay and/or motor deficits. Diagnosis Massive hydrocephalus (aqueductal stenosis) P Pearls y Massive hydrocephalus in a neonate is commonly due to obstruction; a thin peripheral cortical mantle is seen. Diagnostic image evaluation of hydranencephaly and pictorially similar entities, with emphasis on computed tomography. Meningiomas are the most common primary adult intracranial tumor and occur more frequently in women. Although intraventricular meningiomas are uncommon, they still represent the most common atrial masses in adults. Meningiomas arise from arachnoid cap cells within the choroid plexus or velum interpositum. They occur most often in children within the atria of the lateral ventricles and less commonly in adults within the fourth ventricle. Central neurocytomas are histologically distinct but similar to oligodendrogliomas. They arise from and have a broad attachment to the septum pellucidum or ventricular wall. Patients may present with ventricular obstruction, visual disturbances, or hormonal changes. Lesions appear as circumscribed, lobulated masses with numerous cysts, often with a "soap bubble" appearance. In addition to being common posterior fossa tumors in kids, ependymomas may also be supratentorial, within the ventricles or brain parenchyma (more common). Subependymomas occur more often in adults within the fourth and lateral ventricles. In the lateral ventricles, they may mimic central neurocytomas with a "bubbly" appearance. Lesions are identified based on interval growth of a subependymal nodule in the characteristic location; enhancement pattern is not a distinguishing feature. Diagnosis Choroid plexus tumor (papilloma) P Pearls y Meningiomas are the most common primary intracranial and intraventricular/atrial tumors in adults. Alcohol is neurotoxic, causing cerebellar and cortical (frontal lobe predominant) degeneration, as well as peripheral polyneuropathies. There is disproportionate involvement of the superior vermis and cerebellum compared to the cerebral hemispheres. Both seizures and long-term anticonvulsant therapy may produce irreversible cerebellar degeneration with disproportionate cerebellar atrophy. Less common associated malignancies include gastrointestinal and genitourinary neoplasms, Hodgkin lymphoma, and neuroblastoma. The cerebellar degeneration is thought to result from autoantibodies to Purkinje fibers or a cytotoxic process associated with T-cells. The paraneoplastic cerebellar degeneration often precedes the diagnosis of a primary tumor. Imaging reveals atrophy of the ventral pons and midbrain with enlargement of the fourth ventricle and widening of the superior and middle cerebellar peduncles. Less pronounced cerebral atrophy preferentially involves the frontal and parietal lobes. Cruciformlike T2 hyperintensity in the pons gives the classic "hot cross bun" sign. Signal abnormality is also seen in the middle cerebellar peduncles and dorsolateral putamen. Patients present with parkinsonian features, ataxia, dysarthria, and autonomic dysfunction. Cross-sectional imaging demonstrates cerebellar atrophy with enlargement of the cerebellar sulci and compensatory enlargement of the fourth ventricle. Intracranial telangiectasias may result in scattered foci of gradient echo susceptibility secondary to microhemorrhages. Occasionally, associated supratentorial white matter demyelination or dysmyelination may be seen. Also known as spinocerebellar ataxia, Friedreich ataxia typically presents in the second decade of life and has both autosomal dominant and recessive forms. Crosssectional imaging demonstrates mild atrophy of the vermis and paravermian structures, a small medulla, and significant atrophy of the spinal cord. Clinically, patients often present with lower extremity ataxia, upper extremity tremors, and kyphoscoliosis. Diagnosis Anticonvulsant therapy (long-term phenytoin use) P Pearls y Alcohol, anticonvulsant therapy, and paraneoplastic syndromes are secondary causes of cerebellar atrophy. Lesions are hyperintense on T2 sequences and most commonly located along the posterolateral aspect of the cord. There is little edema, if any; enhancement may be seen during periods of active demyelination. The plaques are typically small, usually spanning less than two vertebral bodies in length. It may be caused by a variety of factors, including infectious, ischemic, autoimmune (collagen vascular diseases), demyelinating, and paraneoplastic processes. Imaging shows abnormal cord signal, which may affect the whole cord at that level; enhancement is variable. The most common intramedullary neoplasms include ependymomas, which are most common in adults, and astrocytomas, which are more common in children. Ependymomas may be either myxopapillary at the caudal end of the cord or cellular within the central portion of the cord. Both neoplasms may extend up to 4 vertebral bodies in length, although astrocytomas may rarely be holocord. In general, ependymomas are more circumscribed and heterogeneous; intratumoral cysts and cord edema are commonly seen. Astrocytomas are typically more ill-defined and diffuse, causing fusiform cord expansion. Cord contusions occur with trauma and present with acute-onset neurologic deficits. There is increased T2 signal intensity and edema within the involved segment of the cord. Secondary findings of trauma include spinal fractures, marrow edema, ligamentous injury, and soft-tissue injuries. The spinal cord arterial supply consists of a single anterior spinal artery and paired posterior spinal arteries. Cord infarcts are multifactorial and may be caused by arterial occlusion, usually the anterior spinal artery, or venous hypertension. Imaging findings of arterial infarcts include central increased T2 signal intensity involving the cord gray matter, as well as cord edema and swelling. Venous edema and infarcts are less specific in their imaging pattern and are often due to spinal dural arteriovenous fistulas or underlying causes of impaired venous drainage. Imaging demonstrates signal abnormality involving the posterior columns with a characteristic "inverted V" appearance on axial sequences. The mass (c) is hypointense on T1-weighted sequences and (d) demonstrates mild homogeneous enhancement after contrast administration. Cerebrovascular disease is common in adults and most often results from thromboembolic disease. Gyral or patchy enhancement may be seen in the subacute phase, beginning as early as 2 days and peaking around 10 to 14 days. Perfusion imaging is useful in identifying the penumbra, which represents viable parenchyma at risk of infarct. Fibrillary astrocytoma often presents with indistinct or less commonly well-defined signal abnormality centered in the white matter with or without cortical involvement. Anaplastic astrocytoma is more aggressive with regions of increased perfusion, edema, and enhancement. Restricted diffusion is not seen, unless there is focal progression to a highgrade tumor. They are centered within the subcortical white matter and commonly extend to the cortex. Cerebritis refers to focal infection of the brain parenchyma and may result from hematogenous spread, direct spread, or as a complication of meningitis. Cerebral contusions result from trauma as the brain contacts the skull base or dural reflections. Common locations include the inferior frontal lobes, anterior temporal lobes, and parasagittal locations. Contusions beneath the site of impact are referred to as coup injuries, while those on the opposite side of injury are referred to as contrecoup injuries. It typically occurs with status epilepticus where seizure activity lasts for 30 minutes. Diagnosis Neoplasm (astrocytoma) P Pearls y Infarcts often result from thromboembolic disease; vasculitis and dissection are common in younger patients. Relative increased signal intensity within the visualized sacrum corresponds to loss of fat suppression. Disc extrusion refers to herniations with migration of the disc fragment within the anterior epidural space. The extruded fragment is usually similar in signal intensity and in continuity with the parent disc, unless it becomes sequestered. Although sequestered discs often remain in the anterior epidural space, they may occasionally migrate laterally or even posteriorly. Epidural hematomas may occur spontaneously or result from trauma, transient venous hypertension (cough), iatrogenia, or coagulopathy.

Active demyelination may enhance in a nodular or ring pattern with the open ring toward the overlying cortex gastritis symptoms sweating quality 150 mg ranitidine. Leukodystrophies are a group of rare metabolic disorders characterized by dysmyelination secondary to accumulation of toxic metabolites as a result of enzyme deficiencies (lysosomal gastritis x helicobacter pylori order genuine ranitidine online, peroxisomal chronic gastritis forum purchase ranitidine 150mg otc, or mitochondrial disorders) gastritis diet ����������� order 150 mg ranitidine mastercard. Patients present most commonly at an early age with visual or behavioral disturbances chronic gastritis mucosa buy ranitidine with visa. Metachromatic leukodystrophy has a predilection for the occipital lobes and splenium of the corpus callosum with sparing of subcortical U-fibers atrophic gastritis symptoms diarrhea generic ranitidine 300mg visa. Adrenoleukodystrophy has a similar pattern, commonly affects males (x-linked), also affects the adrenal glands, and involves subcortical U-fibers in late stages of the disease. Both Alexander and Canavan diseases often result in macrocephaly in addition to the white matter manifestations. Both chemotherapy and radiation therapy may result in confluent regions of signal abnormality, predominantly involving the white matter. Chemotherapy changes are typically bilateral and symmetric; radiation changes correspond to a treatment field. High-grade gliomas, lymphoma, and metastases represent the majority of ring-enhancing tumors. Lesions are typically solitary with marked mass effect, surrounding vasogenic edema, thick irregular peripheral enhancement, and central necrosis. The tumor is predominantly T2 hyperintense; regions of hemorrhage and restricted diffusion (due to high cellularity) are common. There is solid enhancement in immunocompetent patients; ring enhancement is seen following treatment or in immunosuppressed patients. There is often pronounced edema, except for cortical metastases which show little edema. Abscesses result from hematogenous spread; direct spread from sinonasal or otomastoid infections, trauma, or surgery; or as a complication of meningitis. Abscesses have a T2 hypointense capsule which is thinner toward the ventricles (prone to intraventricular rupture) with smooth rim enhancement and surrounding vasogenic edema. Toxoplasmosis, a parasitic infection in immunosuppressed patients, does not typically show restricted diffusion. Cortically based infarcts are typically located in a vascular distribution; deep infarcts may be more difficult to characterize. The presence of edema, mass effect, hemorrhagic transformation, and subacute enhancement may mimic a mass lesion, especially if ring enhancing. Infarcts show restricted diffusion acutely, which may persist into the subacute phase. This is helpful but nonspecific, as abscesses and cellular neoplasms may also show restricted diffusion. High specificity locations include the corpus callosum, optic pathways, and posterior fossa. The enhancement pattern may be nodular or "open-ring" with the open portion facing the cortex. A history of trauma is important in differentiating a contusion from other ring-enhancing lesions. Blood products are present in varying stages, depending on the age of the hematoma. Subacute blood products (intra- or extracellular methemoglobin [MetHb]) are T1 hyperintense. The mass is (b) T2 hyperintense with (c) avid enhancement on T1 postcontrast image with fat suppression. Rarely, large cysts (>15 mm) may produce symptoms secondary to local mass effect with headaches or visual disturbances. Simple cysts follow fluid signal intensity and lack central, solid enhancement; surrounding enhancement involving the cyst wall and within the pineal substance is commonly seen. The cysts may demonstrate increased signal intensity on T1 sequences due to proteinaceous content or occasionally hemorrhage with trauma. Cysts greater than 10 mm are often followed with serial imaging to ensure stability, especially if atypical features are identified. Presenting symptoms are often secondary to mass effect resulting in obstructive hydrocephalus, Parinaud syndrome (paralysis of upward gaze), or endocrine dysfunction. Yolk sac tumors may be cystic and associated with elevated levels of alpha-fetoprotein. Choriocarcinomas have a propensity to bleed and are associated with elevated levels of human chorionic gonadotropin. Pineoblastomas are more malignant with a peak incidence in the first decade of life. When calcifications occur, they are typically along the periphery in an "exploded" pattern. Tectal gliomas are slow growing, lowgrade astrocytomas which occur primarily in children. Imaging reveals bulbous enlargement of the tectal plate with narrowing or obstruction of the cerebral aqueduct. The cystic component along the superior aspect of the mass is T2 (a) and mildly T1 (b) hyperintense. The smaller solid component of the mass inferiorly demonstrates regions of enhancement on the T1 postcontrast image with fat suppression (c). Pediatric adamantinomatous craniopharyngiomas present as multicystic suprasellar masses which may extend into the sella, anterior and middle cranial fossae, and retroclival regions. In contrast, the adult variant (papillary) most commonly presents as a solid enhancing suprasellar mass without calcifications. They occur most often in the pineal region, followed by the suprasellar region and are typically midline. Germinomas are the most common subtype and present as infiltrating sellar and/or suprasellar masses which typically follow gray matter signal and homogeneously enhance. With sellar involvement, there is often absence of the posterior pituitary bright spot on precontrast T1 images. Teratomas are more heterogeneous and usually have regions of macroscopic fat and calcification. Rathke cleft cysts are nonneoplastic lesions which arise from remnants of Rathke cleft. There is no internal enhancement, but a rim of enhancing pituitary gland is often seen. Optic nerve gliomas are low-grade tumors that often occur between 5 and 15 years of age. Hypothalamic hamartomas are benign lesions that occur in children with gelastic seizures or precocious puberty. The hamartomas are isointense to gray matter on T1 and iso- to hyperintense on T2 sequences. No enhancement should be seen; the presence of enhancement suggests a hypothalamic glioma rather than hamartoma. Diagnosis Craniopharyngioma P Pearls y Pediatric craniopharyngiomas present as multilobulated, multicystic masses with regions of calcification. The mass extends into the right cerebellopontine angle and prepontine cistern with leftward displacement and compression of the brainstem. As with all posterior fossa tumors, patients often present with headache or symptoms related to obstructive hydrocephalus. The tumor typically arises from the superior medullary velum or roof of fourth ventricle. Although characteristically midline, lateral (cerebellar hemisphere) origin may be seen in older children and young adults. They are T1 hypointense and T2 iso- to hyperintense with heterogeneous enhancement. Cystic changes occur in half of the cases; calcification occurs in approximately 20%. Subarachnoid seeding is noted in up to one-third of the cases at presentation; therefore, evaluation of the neuroaxis is required prior to surgical resection. The tumor arises from the cerebellar hemisphere; therefore, it is typically off-midline. A less common imaging appearance includes a solid mass with a cystic/necrotic center. Ependymoma is a slow-growing, midline posterior fossa tumor that originates along the floor of the fourth ventricle. It characteristically squeezes through the fourth ventricle foramina into the foramen magnum, cerebellopontine angle, or cisterna magna. Two-thirds arise from the fourth ventricle; one-third of the cases are supratentorial and centered in the brain parenchyma. Brainstem glioma represents approximately 10 to 20% of pediatric brain tumors and commonly presents within the first and second decades of life. Higher grade regions demonstrate restricted diffusion, increased enhancement, and increased perfusion. It often presents in the first few years of life with most located in the posterior fossa and the remainder occurring supratentorially. Its appearance on gross examination and imaging is nearly identical to medulloblastoma. Prognosis is dismal; mean survival is less than 6 months if younger than 3 years at the time of presentation. Neuroimaging of pediatric posterior fossa tumors including review of the literature. Ischemic changes commonly affect the posterior fossa and may have a masslike appearance. The morphology of an infarct is often wedge-shaped and corresponds to a vascular territory (posterior inferior, anterior inferior, and superior cerebellar arteries). Edema, mass effect, hemorrhagic transformation, and subacute enhancement may mimic a mass. Metastatic disease represents the most common posterior fossa parenchymal neoplasm in middle-aged and older adults. Tumors are typically solid; cystic change and calcification occasionally occur with mucinous adenocarcinomas. Hemorrhagic metastases, which may occur with breast, lung, renal cell, thyroid, melanoma, and choriocarcinoma, tend to have strong enhancement and a hemosiderin rim. Renal cell carcinoma metastases may mimic hemangioblastoma, as they are very vascular. Ninety to 95% occur within the posterior fossa, typically within the cerebellar hemispheres, while 5 to 10% are supratentorial. Larger lesions present as cystic masses with enhancing mural nodules (similar to juvenile pilocytic astrocytoma) which abut the pial surface; smaller lesions commonly present as solid enhancing masses. Solid components avidly enhance, abut the pial surface, and may demonstrate flow voids. When identified, the entire neuroaxis should be imaged to look for additional cord lesions. Hypertensive hemorrhage commonly involves the posterior fossa, to include the pons and cerebellar hemispheres. Gradient echo and susceptibility weighted imaging often identify additional foci of microhemorrhage associated with hypertension in the lentiform nuclei and thalami. Diagnosis Subacute posterior inferior cerebellar artery territory infarct P Pearls y Ischemia commonly affects the posterior fossa, follows a vascular distribution, and has restricted diffusion. Microvascular ischemic disease is common in the elderly and can be advanced for age. Vasculitis most often presents as multifocal gray and white matter lesions which are bilateral, usually cortical or subcortical and often involve the basal ganglia and thalami. Lesions are bilateral and asymmetric, often involving the optic pathways, corpus callosum, cerebellum, cerebellar peduncles (brachium pontis), and brainstem/cord. There may be transient nodular or "open ring" enhancement during active demyelination. Lyme disease is a tick-borne illness caused by the spirochete Borrelia burgdorferi. Gliomatosis cerebri is an infiltrating glial tumor which involves three or more lobes and may be bilateral. Although centered within the hemispheric white matter, the cortex may also be involved. There is relative preservation of the underlying brain architecture and no or minimal enhancement. Anaplastic astrocytoma may be more discrete, with enhancement ranging from none to focal or patchy. Enhancement is typically homogeneous unless the patient is immunocompromised or steroids have been administered; then there may be ring enhancement. Chemotherapy changes are typically bilateral and symmetric, while radiation changes most often correspond to a treatment field. Diagnosis Treatment-related leukoencephalopathy (chemotherapy) P Pearls y Demyelinating processes are a common cause of white matter lesions and may be confluent when severe. There is hypoplasia of the cerebellar vermis inferiorly, as well as an enlarged posterior fossa with elevation of the torcula (confluence of sinuses) above the lambdoid suture (torcular-lambdoid inversion). It can usually be differentiated from an arachnoid cyst or Dandy-Walker malformation by the normal appearance and size of the posterior fossa, normal cerebellar vermis and fourth ventricle, minimal to no mass effect, and the presence of internal vessels and the falx cerebelli. Although typically asymptomatic and discovered incidentally, they may exert local mass effect.

An infected branchial cleft cyst appears as a tender gastritis and gastroparesis diet ranitidine 150 mg cheap, inflammatory mass located along the anterior border of the sternocleidomastoid muscle chronic gastritis food allergy order ranitidine with mastercard. Thyroglossal cysts (A) arise from remnants of the thyroglossal duct and present as midline neck masses gastritis surgery order cheapest ranitidine and ranitidine. Parathyroid adenomas (B) commonly present with hypercalcemia diet untuk gastritis akut purchase ranitidine without prescription, and aspiration typically reveals crystal-clear fluid gastritis diet ���� 300 mg ranitidine otc. A solitary gastritis symptoms upper back pain buy 300 mg ranitidine, autonomously functioning thyroid nodule is referred to as toxic adenoma (D). Symptoms of weight loss, weakness, shortness of breath, palpitations, tachycardia, and heat intolerance are noted. Location of the tumor in this patient is highly unlikely for thymoma (E), which normally manifests as an anterior mediastinal mass with or without local invasion. Correct: Ectoderm (A) History of an infant with tracheomalacia (A, flaccid tracheal cartilage) includes wheezing that does not improve with bronchodilator therapy. Unlike infants with bronchiolitis (C), asthma (D), or cystic fibrosis (E), these infants maintain normal oxygenation. Correct: Pharyngeal arch 6 (E) Laryngomalacia results from malformed laryngeal cartilages due to defective neural crest cell migration within the 6th pharyngeal arches. Skeletal elements primarily derived from the 1st pharyngeal arches (A) are facial bones. Skeletal elements primarily derived from the 2nd pharyngeal arches (B) are the stapes and the lesser cornu and upper part of the body of the hyoid. Skeletal elements primarily derived from the 3rd pharyngeal arches (C) are the greater cornu and lower part of the body of the hyoid. Correct: Loss of general sensation over a small part of the external acoustic meatus (E) the facial nerve exits the skull through the stylomastoid foramen. As the nerve exits the stylomastoid foramen, it gives off a sensory branch that supplies part of the external acoustic meatus and tympanic membrane. Muscles that develop from the 1st pharyngeal arch (A) are supplied by the trigeminal nerve. It is supplied by a branch of the facial nerve given off from its mastoid segment (course from pyramidal eminence to stylomastoid foramen), which is proximal to the stylomastoid foramen. Taste fibers for the tip of the tongue (C) are supplied by the chorda tympani branch of the facial nerve, which is also given off from its mastoid segment and hence will be unaffected by the fracture. Taste fibers for the vallate papillae (D) are supplied by the glossopharyngeal nerve. Correct: Primary palate (B) Branchial cleft cysts commonly arise from a failure of obliteration of the second branchial cleft in embryonic development. The second arch grows caudally and, ultimately, covers the third and fourth arches. The buried clefts become ectoderm-lined cavities, which normally involute around week 7 of development. Pharyngeal pouches are endoderm-lined (B, C) with internal indentations between the arches. Correct: Laryngomalacia (B) the infant is suffering from laryngomalacia, which is defined as the collapse of supraglottic structures during inspiration. Tracheomalacia (A), bronchiolitis (C), asthma (D), and cystic fibrosis (E) patients present with wheezing (noisy expiration), but not stridor. Structures formed from the medial nasal process (prominence) are the crest and tip of the nose (columella), the philtrum and lateral portion of the upper lip, primary palate, and upper incisors. The secondary palate (C) is formed by fusion of the right and left palatine processes, off the respective maxillary prominences. Correct: Third pharyngeal pouch (C) the superior laryngeal nerve supplies the 4th pharyngeal arch. Muscles derived from the arch are the cricothyroid, levator veli palatini, and constrictors of pharynx. The tensor tympani (A) and tensor veli palatini (B) derive from the 1st pharyngeal arch. The transverse arytenoid (D), an intrinsic muscle of the larynx, derives from the 6th pharyngeal arch. Correct: Mandible bone (C) the thymus and inferior parathyroid glands develop from the third pharyngeal pouch. The thyroid gland develops from endodermal invagination from the foramen cecum (E). Laryngeal electromyography has been the gold standard in diagnosis due to the capability to detect signs of denervation. The external innervates the cricothyroid muscle, which controls longitudinal tension of the vocal folds and voice pitch. The internal supplies sensory fibers to part of the larynx above the vocal cord, hence the laryngeal inlet. The sternothyroid (A) muscle is supplied by the ansa cervicalis of the cervical plexus receiving fibers from the ventral rami of C1-C3 spinal nerves. The thyrohyoid muscle (B) is supplied by a branch from anterior rami of C1 spinal nerve. Paralysis of the thyroarytenoid muscle (C) and anesthesia of the laryngotracheal junction (E) would result from recurrent laryngeal nerve palsy. This is ruled out in the patient by finding an intact posterior cricoarytenoid muscle, which is supplied by the recurrent laryngeal nerve. The mandible develops from the 1st pharyngeal arch, and mandibular hypoplasia is a common finding in the syndrome. Greater (A, 3rd pharyngeal arch derivative) and lesser (B, 2nd pharyngeal arch derivative) horns of hyoid bone are not commonly affected; constrictors of the pharynx (D) or thyroid cartilage (E), both being 4th pharyngeal arch derivatives, are not affected either. Correct: Tensor veli palatini (C) the child is suffering from paralysis of the left lateral pterygoid muscle, consequent to a neuropathy affecting the mandibular division of the trigeminal nerve. The right and left lateral pterygoid muscles function together to cause symmetrical anterior movement of the mandible during opening of the mouth. In unilateral lateral pterygoid muscle palsy, the jaw deviates toward the paralyzed side. Because the trigeminal nerve supplies the 1st pharyngeal arch, all muscles (including tensor veli palatini) derived from the arch would eventually undergo degeneration. Orbicularis oris (A) and orbicularis oculi (B) are derived from the 2nd pharyngeal arch, hence supplied by the facial nerve. Levator veli palatini (D) is derived from the 4th pharyngeal arch, hence supplied by the vagus nerve. Stylopharyngeus (E) is derived from the 3rd pharyngeal arch, hence supplied by the glossopharyngeal nerve. Analyze the etiopathogenesis, clinical features, diagnosis, and complications of neural tube defects. Describe the development, structure, and functions of central and peripheral glia. Analyze the etiopathogenesis, clinical features, and diagnosis of glossopharyngeal neuralgia. Analyze the etiopathogenesis, clinical features, diagnosis, and complications of congenital aqueductal stenosis. Define the primary and secondary brain vesicles and trace their derivatives in human. Analyze the etiopathogenesis, clinical features, and diagnosis of holoprosencephaly. Analyze the etiopathogenesis, clinical features, and diagnosis of tethered cord syndrome. Analyze the etiopathogenesis, clinical features, and diagnosis of Dandy-Walker malformation. A 3-day-old male neonate presents with significant difficulty with sucking and swallowing. A 60-year-old woman is undergoing follow-up neurological examination during her recovery from a stroke. Which of the following is the source of cell bodies involved in the primary afferent limb of this reflex A 6-month-old baby presents with microcephaly, hypotonia, profound mental retardation, and seizures. A 23-year-old woman presents with a dimple and a tuft of hair over the lower lumbar region of the vertebral column. There were no sensorimotor deficits noted during a detailed neurological examination. A plain radiograph revealed missing neural arches involving several lumbar vertebrae. Antenatal diagnosis of this condition could have been possible by noting decreased fetoprotein levels in maternal serum. Prevention of this condition might have been possible by maternal consumption of folic acid. A 26-year-old first-time mother suffers from a viral illness during the third week of her pregnancy. The virus has a known inclination toward cells that form chromaffin cells of the adrenal medulla. Modulation of neuronal activities by buffering K+ concentration in the extracellular space of the brain E. A 48-year-old man presents with a 2-year history of severe, transient, and stabbing pain that initiates in the right side of his throat. It gradually radiates to the base of his tongue, right ear, and occasionally beneath the angle of his right jaw. Which of the specific segments of the central nervous system does the affected structure in the individual connect to Myelencephalon Consider the following case for questions 9 to 10: A 3-day-old girl presents with enlarging head size, bulging fontanelles, and gaping cranial sutures. Postnatal magnetic resonance imaging is suggestive of congenital aqueductal stenosis. Which of the following embryonic segments contributes to the development of the obstructed structure in her A 39-year-old woman suffers a stroke involving the posterior inferior cerebellar artery that causes specific damage to the brainstem special somatic afferent column. A 48-year-old woman presents with loss of taste sensation from the pharyngeal part of her tongue. Which of the following is the embryonic source for cell bodies of the involved primary afferent neurons A 28-week fetal ultrasound in a 20-year-old pregnant mother showed absent interhemispheric fissure and corpus callosum, fused thalami, and fused cerebral hemispheres with one cerebral ventricle. The neonate, delivered preterm at 32 weeks, was born with cyclopia and macroglossia. A second trimester fetal ultrasound in a 28-year-old woman shows a midline cystic mass overlying the occipital bone that contains echoes from herniated brain tissue. Laboratory findings for her were within normal limits other than elevated serum -fetoprotein. Her sensation of pain and touch was lost in the lateral side of the foot with saddle type of perianal anesthesia. A second-trimester fetal ultrasound in a 42-year-old woman suggests a developmental defect affecting the neuroectoderm of the diencephalon segment of the neural tube. Which of the following organs might be at risk in the newborn if the course of the remaining pregnancy stays otherwise uneventful A 48-year-old woman, being treated with colchicine (a drug that arrests mitosis) for chronic gout, finds out that she is 4 weeks pregnant. Cells within which of the following layers of the neural tube in the developing embryo would mostly be affected Fetal ultrasonography reveals a neural mass protruding through arch defects in lower lumbar vertebrae. The cerebellum appears markedly compressed and hypoplastic, and the vermis cannot be displayed. Communication of the 4th ventricle with an abnormally persistent retrocerebellar cyst E. Correct: Chiari type I malformation (A) Chiari malformations are a group of congenital hindbrain abnormalities affecting the structural relationships between the cerebellum, brainstem, the upper cervical cord, and the skull base. In type I, cerebellar tonsils are displaced into the upper cervical canal through the foramen magnum. Dandy-Walker malformation (C) is characterized by agenesis or hypoplasia of the cerebellar vermis, cystic dilatation of the fourth ventricle, and enlargement of the posterior fossa. Holoprosencephaly (D) occurs when the prosencephalon fails to cleave down the midline such that the telencephalon contains a single ventricle. Lissencephaly (E) is a heterogeneous group of disorders of cortical formation characterized by a smooth brain, with absent or hypoplastic sulci. Correct: Failure of migration of neuroblasts (E) the neonate is suffering from lissencephaly (absence of cortical gyri) and possibly from neuronal heterotopia (normal neurons in abnormal locations), both of which are caused by neuroblast migration defects. Failure of closure of the rostral (B) or caudal (C) neuropore causes neural tube defects; failure of migration of neural crest cells (D) are termed neurocristopathies. Correct: Prevention of this condition might have been possible by maternal consumption of folic acid. This occurs due to failure of closure of one or several vertebral arches posteriorly; the meninges and spinal cord are normal. Incomplete cover of dura and arachnoid mater (A, meningocele) or cystic dilatation of several segments of the spinal cord (B, syringomyelia) is highly unlikely to be asymptomatic. Gastrulation (E) is the process of forming three definitive germ layers in the embryo.

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