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This slender nerve cholesterol medication classes buy online tricor, which is often avulsed when the brain is removed at autopsy cholesterol medication zoloft buy 160 mg tricor amex, runs along the clivus cholesterol medication weight gain best order tricor, through the tentorial opening cholesterol definition wikipedia buy cheapest tricor and tricor, into the cavernous sinus and superior orbital fissure, on its way to the lateral rectus muscle. The axons emerge from the anterior medullary vellum just behind the inferior colliculi, then wrap around the brainstem, pass through the tentorial opening, enter the cavernous sinus, and travel through the superior orbital fissure to innervate the superior oblique muscle. Unilateral or even bilateral abducens palsy is commonly seen as a false localizing sign in patients with increased intracranial pressure. Although the long intracranial course of the nerve is often cited as the cause of its predisposition to injury, the trochlear nerve (which is rarely injured by diffusely increased intracranial pressure) is actually longer,94 and the sharp bend of the abducens nerve as it enters the cavernous sinus may play a more decisive role. From a clinical point of view, however, it is important to remember that isolated unilateral or bilateral abducens palsy does not necessarily indicate a site of injury. The emergence of the trochlear nerve from the dorsal midbrain just behind the inferior colliculus makes it prone to injury by the tentorial edge (which runs along the adjacent superior surface of the cerebellum) in cases of severe head trauma. Thus, trochlear nerve palsy after head trauma does not necessarily represent a focal brainstem injury (although the dorsal brainstem at this level may be damaged by the same process). The course of all three ocular motor nerves through the cavernous sinus and superior orbital fissure means that they are often damaged in combination by lesions at these sites. Thus, a lesion of all three of these nerves unilaterally indicates injury in the cavernous sinus or superior orbital fissure rather than the brainstem. Head trauma causing a blowout fracture of the orbit may trap the eye muscles, resulting in abnormalities of ocular motility unrelated to any underlying brain injury. These afferents arise from cortical, tectal, and tegmental oculomotor systems, as well as directly from the vestibular system and vestibulocerebellum. In principle, these classes of afferents are not greatly different from the types of inputs that control alpha-motor neurons concerned with striated muscles, except the oculomotor muscles do not contain muscle spindles and hence there is no somesthetic feedback. The oculomotor nuclei are surrounded by areas of the brainstem tegmentum containing premotor cell groups that coordinate eye movements. In addition, neurons in the dorsal pontine nuclei relay smooth pursuit signals to the flocculus, and the medial vestibular nucleus and flocculus are both important for holding eccentric gaze. Axons from these latter neurons cross the midline at the level of the abducens nucleus and ascend on the contralateral side of the brainstem to allow conjugate lateral gaze. Thus, pontine tegmental lesions typically result in the inability to move the eyes to the ipsilateral side of space (lateral gaze palsy). A premotor area for vergence eye movements is found at the rostral tip of this region, near the midbrain-diencephalic junction. Unilateral lesions of the rostral interstitial nuclei typically reduce vertical saccades as well as causing torsional nystagmus. Each superior colliculus contains a map of the visual world on the contralateral side of space, and electrical stimulation of a specific point in this visual map will command a saccade to the corresponding point in space. In nonmammalian vertebrates, such as frogs, this area is called the optic tectum and is the principal site for directing eye movement; in mammals, it comes largely under the control of the cortical system for directing eye movements. Unlike neurons in the primary motor cortex, which fire in relation to movements of the limbs in particular directions at particular joints, recordings from area 8 neurons in awake, behaving monkeys indicate that they do not fire during most random saccadic eye movements. However, they are engaged during tasks that require a saccade to a particular part of space only when the saccadic eye movement is part of a behavioral sequence that is rewarded. In this respect, neurons in area 8 are more similar to those in areas of the prefrontal cortex that are involved in planning movements toward the opposite side of space. Area 8 projects widely to both the superior colliculus as well as the premotor areas for vertical and lateral eye movements, and to the ocular motor nuclei themselves. Thus, following an object that travels from the left to the right engages the right parietal cortex (area 7) to fix attention on the object, the right area 8 to produce a saccade to pick it up, the right occipital cortex to follow the object to the right, and ultimately the left occipital cortex as well to see the object as it enters the right side of space. Thus, following moving stripes to the right, as in testing optokinetic nystagmus, engages a number of important cortical as well as brainstem pathways necessary to produce eye movements. Hence, although the test is fairly sensitive for picking up oculomotor problems at a cortical and brainstem level, the interpretation of failure of optokinetic nystagmus is a complex process. In addition to these motor inputs, the ocular motor neurons also receive sensory inputs to guide them. Although there are no spindles in the ocular motor muscles to provide somatic sensory feedback, the ocular motor nuclei depend on two different types of sensory feedback. Second, the ocular motor nuclei receive direct and relayed inputs from the vestibular system. The abducens nucleus is located at the same level as the vestibular complex, and it receives inputs from the medial and superior vestibular nuclei. These inputs from the vestibular system allow both horizontal and vertical eye movements (vestibulo-ocular reflexes) in response to vestibular stimulation. Another sensory input necessary for the brain to calculate its position in space is head position and movement. The vestibulocerebellum, including the flocculus, paraflocculus, and nodulus, receives ex- tensive vestibular input as well as somatosensory and visual afferents. The vestibulocerebellum is also critical in learning new relationships between eye movements and visual displacement. Lesions of the vestibulocerebellum cause ocular dysmetria (inability to perform accurate saccades), ocular flutter (rapid to-andfro eye movements), and opsoclonus (chaotic eye movements). The abducting eye shows horizontal gaze-evoked nystagmus (slow phase toward the midline, rapid jerks laterally), while the adducting eye stops in the midline (if the lesion is complete) or fails to fully adduct (if it is partial). Vertical saccades, however, are implemented by the superior colliculus inputs to the rostral interstitial nucleus of Cajal, and are intact. The Ocular Motor Examination the examination of the ocular motor system in awake, alert subjects involves testing both voluntary and reflex eye movements. In patients with stupor or coma, testing of reflex eyelid and ocular movements must suffice. The eyelids at rest in coma, as in sleep, are maintained in a closed position by tonic contraction of the orbicularis oculi muscles. The eyelids of a comatose patient close smoothly and gradually, a movement that cannot be duplicated by an awake individual simulating unconsciousness. Absence of tone or failure to close either eyelid can indicate facial motor weakness. Blepharospasm, or strong resistance to eyelid opening and then rapid closure, is usually voluntary, suggesting that the patient is not truly comatose. However, lethargic patients with either metabolic or structural lesions may resist eye opening, as do some patients with a nondominant parietal lobe infarct. In patients with unilateral forebrain infarcts, the ptosis is often ipsilateral to hemiparesis. Spontaneous blinking usually is lost in coma as a function of the depressed level of consciousness and concomitant eye closure. However, in persistent vegetative state, it may return during cycles of eye opening (Chapter 9). Blinking in response to a loud sound or a bright light implies that the afferent sensory pathways are intact to the brainstem, but does not necessarily mean that they are active at a forebrain level. Even patients with complete destruction of the visual cortex may recover reflex blink responses to light,107 but not to threat. The corneal reflex can be performed by approaching the eye from the side with a wisp of cotton that is then gently applied to the sclera and pulled across it to touch the corneal surface. Corneal trauma can be completely avoided by testing the corneal reflex with sterile saline. Two to three drops of sterile saline are dropped on the cornea from a height of 4 to 6 inches. However, some patients who wear contact lenses may have permanent suppression of the corneal reflex. A small flashlight or bright ophthalmoscope held about 50 cm from the face and shined toward the eyes of the patient should reflect off the same point in the cornea of each eye if the gaze is conjugate. If it is possible to obtain a history, ask about eye movements, as a congenital strabismus may be misinterpreted as dysconjugate eye movements due to a brainstem lesion. Slowly roving eye movements are typical of metabolic encephalopathy, and if conjugate, they imply an intact ocular motor system. The head is rotated first in a lateral direction to either side while holding the eyelids open. This can be done by grasping the head on either side with both hands and using the thumbs to reach across to the eyelids and hold them open.

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Grossly acute gastritis appears as multiple cholesterol ratio very low purchase genuine tricor on line, scattered cholesterol levels what is normal order tricor toronto, punctate (less than 1 cm) hemorrhagic areas in the gastric mucosa hdl cholesterol ratio and risk purchase tricor with a visa. This is helpful in dif- Gastrointestinal System Answers 327 ferentiating acute gastritis from peptic ulcers cholesterol test blood donation buy tricor australia, which tend to be solitary and larger. Microscopically the gastric mucosa from a patient with acute gastritis is likely to reveal mucosal erosions, scattered neutrophils, edema, and possibly hemorrhage. It is important to realize that the presence of neutrophils within the glandular epithelium indicates active inflammation and may be the main type of inflammation present (acute gastritis), or may be combined with more numerous chronic inflammations (active chronic gastritis). Chronic gastritis is divided into subgroups based either on etiology (immunologic or infectious), location (antrum or body), histopathology, or clinical features. The therapy for Helicobacter is either triple therapy (metronidazole, bismuth salicylate, and either amoxicillin or tetracycline) or double therapy (omeprazole and clarithromycin). In contrast, autoimmune gastritis, also known as diffuse corporal atrophic gastritis or type A atrophic gastritis, is characterized by the presence of autoimmune antibodies including parietal cell antibodies and intrinsic factor antibodies. Pernicious anemia is the result of decreased intrinsic factor, which in turn produces a vitamin B12 deficiency. This vitamin deficiency causes megaloblastic anemia and subacute combined disease of the spinal cord. Histologically there is diffuse atrophy (reduced mucosal thickness), gland loss, widespread intestinal metaplasia, and variable chronic and acute inflammation. These changes are found predominately in the body-fundus mucosa (usually absent in the antrum). There is an increased risk for gastric cancer, but these patients do not develop peptic ulcers. Acute gastric ulcers are stress ulcers that are really ero- 328 Pathology sions and not true ulcers. Certain gross and microscopic characteristics help to differentiate benign peptic ulcers from malignant ulcers. Benign peptic ulcers tend to be round and regular with punched-out straight walls. Histologically, the surface of the ulcer shows acute inflammation and necrotic fibrinoid debris, while the base has active granulation tissue overlying a fibrous scar. The gastric epithelium adjacent to the ulcer is reactive and is characterized by numerous mitoses and epithelial cells with prominent nucleoli. In contrast, malignant ulcers grossly are irregular with raised irregular margins. Peptic ulcers are due to the effects of acid and may occur anywhere in the gastrointestinal tract exposed to acid-peptic activity. Over 98% of cases occur in the stomach or duodenum, with duodenal cases outnumbering gastric cases 4 to 1. Ulcers associated with Zollinger-Ellison syndrome are typically multiple and frequently involve distal duodenum and jejunum. Gastric ulceration typically occurs in a setting of normo- or hypochlorhydria with abnormality of mucosal defense mechanisms, back-diffusion of acid, and possibly local ischemia. The treatment of peptic ulcers involves trying to decrease the effects of gastric acid. There are several types of drugs that can be used to treat peptic ulcers, such as cimetidine and omeprazole. Because food neutralizes acid within the stomach and relieves the typical epigastric pain of peptic ulcer disease, patients are advised to eat frequent small meals. Additional therapeutic measures include abstaining from substances or actions that increase gastric acid production, such as coffee, alcohol, and prostaglandin production inhibitors, which include aspirin, indomethacin, ibuprofen, and smoking. In these tumors, intracellular mucin vacuoles coalesce and distend the cytoplasm of tumor cells, which compresses the nucleus toward the edge of the cell and creates a signet ring appearance. Tumors of this type are usually deeply invasive and fall into the category of advanced gastric carcinoma. There is often a striking desmoplasia with thickening and Gastrointestinal System Answers 329 rigidity of the gastric wall, which may result in the so-called linitis plastica ("leather bottle") appearance. Advanced gastric carcinoma is usually located in the pyloroantrum, and the prognosis is poor, with 5-year survival of only 5 to 15%. Rodent ulcer refers to the clinical appearance of some basal cell carcinomas of the skin, while sarcoma botryoides is a malignant vaginal tumor that has a grapelike gross appearance. First-generation migrants carry the risk of their country of origin, but subsequent generations assume the risk of their new country. The decreased rate is due to a decrease in the rate of the intestinal type of gastric cancer. The incidence of the other type, diffuse gastric carcinoma, has not changed recently. It develops very slowly into a frankly invasive lesion and, if detected early and removed, allows a 5-year survival of up to 95% compared with 15% for gastric carcinoma overall. Of all gastric carcinomas, 50 to 60% arise in the pyloroantrum, 10% in the cardia, 10% in the whole organ, and the remainder in other sites. Diffusely infiltrative carcinoma extends widely through the stomach wall, often without producing an intraluminal mass, and incites a marked desmoplastic reaction that results in a thickened, inelastic stomach wall. It represents incomplete involution of the vitellointestinal duct and always arises from the antimesenteric border of the intestine. Heterotopic gastric or pancreatic tissue may be present in about one-half of cases. Peptic ulceration, which occurs as a 330 Pathology result of acid secretion by heterotopic gastric mucosa, is usually located in the adjacent ileum. Complications include perforation, ulceration, intestinal obstruction, intussusception, and neoplasms, including carcinoid tumors. The most common location for this is the terminal ileum, and there are two types of patients who are most at risk, namely weaning infants and adults with a polypoid mass. It is thought that in weaning infants, exposure to new antigens causes hypertrophy of the lymphoid follicles in the terminal ileum and this may result in intussusception. Intussusception produces a classic triad of signs that includes sudden colicky abdominal pain, abdominal distention, and a "currant jelly" stool due to the vascular compromise produced by pulling of the mesentery. In contrast, the combination of fever, leukocytosis, and right lower quadrant abdominal pain is suggestive of acute appendicitis, while fever, leukocytosis, and left lower quadrant abdominal pain is suggestive of acute diverticulitis. A newborn infant with projectile vomiting and midepigastric mass probably has hypertrophic pyloric stenosis, while the acute onset of severe abdominal pain in a male older than 55 might be due to a ruptured abdominal aortic aneurysm. Rotavirus is a major cause of diarrhea in children between the ages of 6 and 24 months. Clinical symptoms consisting of vomiting and watery (secretory) diarrhea begin about 2 days after exposure. Bacterial enterocolitis may be related to either the production of performed toxins, such as with Vibrio cholerae and enterotoxigenic E. It characteristically produces flask-shaped ulcers in the colon and may embolize to the liver, where it produces amebic liver abscesses. Lactase deficiency, a cause of osmotic Gastrointestinal System Answers 331 diarrhea, is very rarely a congenital disorder, but much more commonly is an acquired disorder seen in adults that results in malabsorption of milk and milk products. The onset of symptoms from ulcerative colitis is most commonly apparent between the ages of 20 and 25 years. Histologically it is characterized by villus atrophy with hyperplasia of underlying crypts and increased mitotic activity. The surface epithelium shows disarray of the columnar epithelial cells and increased intraepithelial lymphocytes. Definitive diagnosis in patients with these features on biopsy depends on response to a gluten-free diet and subsequent gluten challenge. A biopsy of the small intestine reveals the mucosal absorptive cells to be vacuolated by lipid (triglyceride) inclusions, and peripheral smear reveals numerous acanthocytes, which are red blood cells that have numerous irregular spikes on their cell surface. The symptoms of malabsorption may be partially reversed by ingestion of medium-chain triglycerides rather than long-chain triglycerides, because these medium-chain triglycerides are absorbed directly into the portal system and are not incorporated into lipoproteins. Tropical and nontropical (celiac) sprue are both characterized by shortened to absent villi in the small intestines (atrophy). Celiac sprue is a disease of malabsorption 332 Pathology related to a sensitivity to gluten, which is found in wheat, oats, barley, and rye. Tropical sprue is an acquired disease found in tropical areas, such as the Caribbean, the Far East, and India. Fibrosis of the lamina propria and submucosa may be seen in patients with systemic sclerosis. Bacterial overgrowth, a result of numerous causes such as the blind loop syndrome, strictures, achlorhydria, or immune deficiencies, may also cause malabsorption.

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If the brain can produce this type of conscious impression in the absence of reality cholesterol foods list cheap tricor online american express, there is no reason to cholesterol levels menopause cheap 160mg tricor with amex think that it requires a physiologic reassembly of other stimuli for presentation to cholesterol normal lab values buy cheap tricor 160mg line a central homunculus cholesterol-lowering foods outdo low-saturated-fat diet purchase online tricor. Rather, consciousness may be conceived as a property of the integrated activity of the two cerebral hemispheres and not in need of a separate physical manifestation. Despite this view of consciousness as an ``emergent' property of hemispheric information processing, the hemispheres do require a mechanism for arriving at a singularity of thought and action. If each of the independent information streams in the cortical parallel processor could separately command motor responses, human movement would be a hopeless confusion of mixed activities. A good example is seen in patients in whom the corpus callosum has been transected to prevent spread of epileptic seizures. The brain requires a funnel to narrow down the choices from all of the possible modes of action to the single plan of motor behavior that will be pursued. All cortical regions provide input to the striatum (caudate, putamen, nucleus accumbens, and olfactory tubercle). By constricting all motor responses that are not specifically activated by this system, the basal ganglia ensure a smooth and steady, unitary stream of action. Basal ganglia disorders that permit too much striatal disinhibition of movement (hyperkinetic movement disorders) result in the emergence of disconnected movements that are outside this unitary stream. The conscious self is prohibited even from seeing two equally likely versions of an optical illusion simultaneously. Rather, the self is aware of the two alternative visual interpretations alternately. Similarly, if it is necessary to pursue two different tasks at the same time, they are pursued alternately rather than simultaneously, until they become so automatic that they can be performed with little conscious thought. The striatal control of thought processes is implemented by the outflow from the ventral striatum to the ventral pallidum, which in turn inhibits the mediodorsal thalamic nucleus, the relay nucleus for the prefrontal cortex. An interesting philosophic question is raised by the hyperkinetic movement disorders, in which the tics, chorea, and athetosis are thought to represent ``involuntary movements. A classic optical illusion, illustrating the inability of the brain to view the same scene simultaneously in two different ways. The image of the ugly, older woman or the pretty younger woman may be seen alternately, but not at the same time, as the same visual elements are used in two different percepts. Instead, the interrelationship of involuntary movements, which the self feels ``compelled' to make, with self-willed movements is complex. Patients with movement disorders often can inhibit the unwanted movements for a while, but feel uncomfortable doing so, and often report pleasurable release when they can carry out the action. Again, the conscious state is best considered as an emergent property of brain function, rather than directing it. Similarly, hyperkinetic movement disorders may be associated with disinhibition of larger scale behaviors and even thought processes. In this view, thought disorders can be conceived as chorea (derailing) and dystonia (fixed delusions) of thought. Release of prefrontal cortex inhibition may even permit it to drive mental imagery, producing hallucinations. Under such conditions, we have a tendency to believe that somehow the conscious self is a homunculus that is being tricked by hallucinatory sensory experiences or is unable to command thought processes. This case shows the residual area of injury at autopsy 7 months after a pontine hemorrhage. Hence, the evaluation of the comatose patient becomes an exercise in applying those principles to the evaluation of a human with brain failure. Structural Lesions That Cause Altered Consciousness in Humans To produce stupor or coma in humans, a disorder must damage or depress the function of either extensive areas of both cerebral hemispheres or the ascending arousal system, including the paramedian region of the upper brainstem or the diencephalon on both sides of the brain. Conversely, unilateral hemispheric lesions, or lesions of the brainstem at the level of the midpons or below, do not cause coma. Lesions of the brainstem may be very large without causing coma if they do not involve the ascending arousal system bilaterally. Even if blood flow or oxygenation is restored after 5 or more minutes, there may be widespread cortical injury and neuronal loss even in the absence of frank infarction. Alternatively, in some patients with less extreme cortical hypoxia, there may be a lucid interval in which the patient appears to recover, followed by a subsequent deterioration. Such a patient is described in the historical vignette on this and the following page. Fortunately, most such cases included pathologic assessment, which is also all too infrequent in modern cases. A companion already had died, apparently the result of an attempted double suicide. The neurologic examination was normal, and an evaluation by a psychiatrist revealed a clear sensorium with ``no evidence of organic brain damage. At home he remained well for 2 days but then became quiet, speaking only when spoken to. Hypoxia typically causes more severe damage to large pyramidal cells in the cerebral cortex and hippocampus compared to surrounding structures. The next day (13 days after the anoxia) he became incontinent and unable to walk, swallow, or chew. He was admitted to a private psychiatric hospital with the diagnosis of depression. Deterioration continued, and 28 days after the initial anoxia he was readmitted to the hospital. His blood pressure was 170/100 mm Hg, pulse 100, respirations 24, and temperature 1018F. His extremities were flexed and rigid, his deep tendon reflexes were hyperactive, and his plantar responses extensor. Histologically, neurons in the motor cortex, hippocampus, cerebellum, and occipital lobes appeared generally well preserved, although a few sections showed minimal cytodegenerative changes and reduction of neurons. Pathologic changes were not present in blood vessels, nor was there any interstitial edema. The striking alteration was diffuse demyelination involving all lobes of the cerebral hemispheres and sparing only the arcuate fibers (the immediately subcortical portion of the cerebral white matter). The condition of delayed postanoxic cerebral demyelination observed in this patient is discussed at greater length in Chapter 5. A series of drawings illustrating levels through the brainstem at which lesions caused impairment of consciousness. For each case, the extent of the injury at each level was plotted, and the colors indicate the number of cases that involved injury to that area. The overlay illustrates the importance of damage to the dorsolateral pontine tegmentum or the paramedian midbrain in causing coma. As a result, it is no exaggeration to say that virtually any deficit due to injury of a discrete cortical area can be mimicked by injury to its thalamic relay nucleus. Hence, thalamic lesions that are sufficiently extensive can produce the same result as bilateral cortical injury. The most common cause of such lesions is the ``tip of the basilar' syndrome, in which vascular occlusion of the perforating arteries that arise from the basilar apex or the first segment of the posterior cerebral arteries can produce bilateral thalamic infarction. Other causes of primarily thalamic damage include thalamic hemorrhage, local infiltrating tumors, and rare cases of diencephalic inflammatory lesions. Examination of her brain at the time of death disclosed unexpectedly widespread thalamic neuronal loss. However, there was also extensive damage to other brain areas, including the cerebral cortex, so that the thalamic damage alone may not have caused the clinical loss of consciousness. On the other hand, thalamic injury is frequently found in patients with brain injuries who eventually enter a persistent vegetative state (Chapter 9). However, the location of the hypothalamus above the pituitary gland results in localized hypothalamic damage in cases of pituitary tumors. Patients with hypothalamic lesions often appear to be hypersomnolent rather than comatose. They may yawn, stretch, or sigh, features that are usually lacking in patients with coma due to brainstem lesions.

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The s ills to repair visceral injuries, control hemorrhage, and maintain hemostasis laparoscopically will help surgeons to minimize morbidities and decrease conversions to laparotomy. This course will explore these s ills through the use of surgical video footage to illustrate the strategies and techniques necessary to overcome the difficulties associated with various anatomy-distorting pathologies. De Los Rios, Juan Diego Villegas-Echeverri Faculty: Jaime Albornoz Valdes, Jorge F. The sessions in Spanish aim to provide current wide-ranging tools for the diagnosis and management of patients suffering this frequent and debilitating condition. The course contents will include pathophysiology, diagnostic approach, and the best strategies for both medical and surgical treatment. This course will highlight various modalities to maximi e exposure, simplify access into the cul-de-sac, insert v T S port and perform simple and di cult vaginal hysterectomies, adnexectomies, and tubal surgery. 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Anderson All Faculty v T S Set- p for Success: ort lacement, Stepwise Procedure for Hysterectomy v T S for the Di cult ysterectomy uestions Answers rea essons earned in v v T S Tubal Surgery for ctopic regnancies, Sterili ation, and Reanastomosis v T S varian Surgery without Concomitant ysterectomy Complications in aginal Surgery: revent, dentify, and Manage uestions Answers Adjourn Support of the aginal Apex During enign ysterectomy 1:25 Surgical Site Infection Bundle 3: 5 3:3 M. This course provides a novel format for exploring ey procedures in modern reproductive surgery. The video session will profile fundamental surgical s ills in minimally invasive reproductive surgery. Miller All Faculty this hands-on simulation course is designed to provide a systematic and comprehensive approach to multiple modalities of minimally invasive myomectomy. This course is intended for both beginning and advanced minimally invasive gynecologic surgeons, including generalists and specialists. Through simulation models, and under the guidance of expert faculty, participants will be provided the opportunity to practice, in a step-by-step surgical approach, hysteroscopic, laparoscopic, and robotic myomectomy, as well as contained tissue extraction techniques. Within each surgical modality, an emphasis will be placed on anatomic planes, surgical techniques, and the utilization of different energy sources and suture types. These simulated approaches will help the surgeons refine their s ills and formulate a wellstrategi ed minimally invasive surgical plan for their patients suffering from uterine myomas. Hologic and the Science of Sure and associated logos are trademarks and/or registered trademarks of Hologic, Inc. She obtained her medical degree from the University of California, San Diego, followed by an internship and residency at the Oregon Health Sciences University. Paraiso is Professor of Obstetrics, Gynecology, and Reproductive Health Sciences at Cleveland Clinic Lerner College of Medicine at Case Western Reserve University and Section Head of Urogynecology and Reconstructive Surgery at the Cleveland Clinic in Cleveland, Ohio. She is committed to work and collaborate with other national and international organizations. Paraiso has pioneered innovative surgeries in traditional and robotic-assisted laparoscopy. She has lectured extensively throughout the world, reviews for 13 major journals, and has authored a vast amount of published work, including 147 peer reviewed publications, 23 book chapters, and one book. She has won many research and teaching awards and was recipient of the 2017 Raymond Lee Lectureship for the American Urogynecologic Society. She enjoys spending precious time with her husband, 2 children, and extended family, traveling, playing various sports, and attending cultural events. 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Beginning with an understanding of the life course impact of endometriosis, we will aim to build the skills necessary to engage our patients with compassion, up-to-date knowledge, and collaboration with other health care providers. Understanding the importance of combining treatment modalities, building a long-term care plan, and disavowing common misconceptions is central to quality care in this space. We have assembled a nationally and internationally recognized panel of hysteroscopic surgeons to review the rationale, patient selection, and hysteroscopic techniques for extirpation of type 2 uterine fibroids. Dionisi, Javier Del Longo, Juan Raul Escalona, Carlos Fernandez Ossadey, Fernando Heredia, William Kondo, Edison R.

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