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Uterine fibroid embolization (UFE), also known as uterine artery embolization, is a minimally invasive procedure that is performed by an Interventional Radiologist (IR), a doctor who uses advanced imaging technology to see inside the body without surgery. UFE is often performed as an outpatient service and offers a much shorter recovery time than surgery. For more information on uterine fibroids and all your treatment options, including UFE,
Plantar warts are hard, grainy growths that usually appear on the heels or balls of your feet, areas that feel the most pressure. This pressure also may cause plantar warts to grow inward beneath a hard, thick layer of skin (callus). Plantar warts are caused by the human papillomavirus (HPV). The virus enters your body through tiny cuts, breaks or other weak spots on the bottom of your feet. Most plantar warts aren't a serious health concern and may not require treatment. But plantar warts can cause discomfort or pain. If self-care treatments for plantar warts don't work, you may want to see your doctor to have them removed.
In this video, the viewer will learn the key aspects of the newborn physical exam, and how to distinguish between normal and abnormal findings.
Direct Links to chapters:
0:00-Intro
1:30-Head
3:49-Face
8:05-Neck
8:30-Chest
10:13-Abdomen
11:01-Groin
13:17-Extremities
14:05-Back
14:47-Neurologic
Please visit: www.openpediatrics.org
OPENPediatrics™ is an interactive digital learning platform for healthcare clinicians sponsored by Boston Children's Hospital and in collaboration with the World Federation of Pediatric Intensive and Critical Care Societies. It is designed to promote the exchange of knowledge between healthcare providers around the world caring for critically ill children in all resource settings. The content includes internationally recognized experts teaching the full range of topics on the care of critically ill children. All content is peer-reviewed and open access-and thus at no expense to the user.
For further information on how to enroll, please email: openpediatrics@childrens.harvard.edu
Please note: OPENPediatrics does not support nor control any related videos in the sidebar, these are placed by Youtube. We apologize for any inconvenience this may cause.
Beating heart or "off pump" coronary artery surgery is the latest revolution in the management coronary disease. It is being embraced world-wide by increasing numbers of surgeons. Many of the advantages are subtle but reduced mortality, stroke, and bleeding as well as earlier discharge are well-established benefits. A cardiac stabiliser is mandatory for this surgery, most are single use only and very expensive, this one is multiple use and is saving many healthcare dollars
Calcium channel blockers prevent calcium from entering cells of the heart and blood vessel walls, resulting in lower blood pressure. Calcium channel blockers, also called calcium antagonists, relax and widen blood vessels by affecting the muscle cells in the arterial walls. Some calcium channel blockers have the added benefit of slowing your heart rate, which can further reduce blood pressure, relieve chest pain (angina) and control an irregular heartbeat. Examples of calcium channel blockers Some calcium channel blockers are available in short-acting and long-acting forms. Short-acting medications work quickly, but their effects last only a few hours. Long-acting medications are slowly released to provide a longer lasting effect. Several calcium channel blockers are available. Which one is best for you depends on your health and the condition being treated. Examples of calcium channel blockers include: Amlodipine (Norvasc) Diltiazem (Cardizem, Tiazac, others) Felodipine Isradipine Nicardipine Nifedipine (Adalat CC, Afeditab CR, Procardia) Nisoldipine (Sular) Verapamil (Calan, Verelan) In some cases, your doctor might prescribe a calcium channel blocker with other high blood pressure medications or with cholesterol-lowering drugs such as statins.
Intrauterine insemination (IUI) is a fertility treatment that involves placing sperm inside a woman's uterus to facilitate fertilization. The goal of IUI is to increase the number of sperm that reach the fallopian tubes and subsequently increase the chance of fertilization
When the colon and rectum are removed (due to ulcerative colitis or familial adenomatous polyposis), another reservoir must be created for bowel contents (stool) to exit the body. Surgically creating a “J” shaped reservoir (called a J-pouch) is an option for selected patients to store and pass stool.
Selective immunoglobulin A deficiency (SIgAD) is a primary immunodeficiency disease and is the most common of the primary antibody deficiencies.[1] Total immunoglobulin A deficiency (IgAD) is defined as an undetectable serum immunoglobulin A (IgA) level at a value < 5 mg/dL (0.05 g/L) in humans. Partial IgAD refers to detectable but decreased IgA levels that are more than 2 standard deviations below normal age-adjusted means.[2, 3] IgAD is commonly associated with normal B lymphocytes in peripheral blood, normal CD4+ and CD8+ T cells, and, usually, normal neutrophil and lymphocyte counts. Anti-IgA autoantibodies of the IgG and/or IgE isotype may be present. Peripheral blood may also be affected by autoimmune cytopenias, eg, autoimmune thrombocytopenia,[4, 5] and patients may have other autoimmune phenomena. IgA was first identified by Graber and Williams in 1952; ten years later, the first patients with IgAD were described. IgAD is a heterogeneous disorder, and the results of intensive study are beginning to elucidate genetic loci and molecular pathogenesis that contribute to various subtypes of this disorder. Several lines of evidence suggest that, in many cases, IgAD and common variable immunodeficiency (CVID) have a common pathogenesis, which is discussed further in Pathophysiology. Other data indicate different genetic risk factors. Family studies show variable inheritance patterns. Familial inheritance of IgAD occurs in approximately 20% of cases,[6] and, within families, IgAD and CVID are associated.[7, 8] Many IgAD patients are asymptomatic (ie, "normal" blood donors) and are identified by finding a laboratory abnormality, without any apparent associated clinical disease. Some patients with IgAD may have the following associated conditions: (1) deficits in one or more immunoglobulin G (IgG) subclasses (this accounts for 20-30% of IgA-deficient patients, many of whom may have total IgG levels within the normal range) or (2) a deficient antibody response to pneumococcal immunization (specific polysaccharide antibody deficiency [SPAD]). Some patients with IgAD later develop CVID, and family members of patients with CVID may have only selective IgAD. Characterization of the receptor for the transmembrane activator and calcium-modulator and cyclophilin ligand interactor (TACI), encoded by the gene TNFRSF13B ( tumor necrosis factor receptor superfamily member 13B), suggests that people with the C104, A181E, and ins204A variants may be at risk for IgAD that progresses to CVID.[9] Primary IgAD is permanent, and below-normal levels have been noted to remain static and persist after 20 years of observation.[10] A recent report documents a rare case of reversion.[11] Environmental factors such as drugs or infections can cause IgAD, but this form is reversible in more than half the cases (see Causes). Although individuals with IgAD have largely been considered healthy, recent studies indicate a higher rate of symptoms. A 20-year follow-up study that compared 204 healthy blood donors with incidentally identified IgAD to 237 healthy subjects with normal IgA levels demonstrated that 80% of IgAD donors and 50% of control subjects had episodes of infections, drug allergy, or autoimmune or atopic disease. Severe respiratory tract infections occurred in 26% of IgAD subjects, in 24% of subjects with decreased IgA levels, and in 8% of control subjects; however, the incidence of life-threatening infections was not increased. IgAD is more common in adult patients with chronic lung disease than in healthy age-matched control subjects.[12] Patients with IgAD are at some increased risk of developing severe reactions after receiving blood products.[13, 14, 15] IgG anti-IgA antibodies may cause severe transfusion reactions if patients with IgAD are given whole blood; therefore, IgA-poor blood or washed red cells are preferred for those patients. IgA-deficient patients with immunoglobulin E (IgE)–class anti-IgA antibodies are at risk for anaphylaxis if they receive blood or intravenous immunoglobulin, but this situation is extremely rare. Individuals with such an unusual profile should receive only low IgA intravenous immunoglobulin preparations. However, caution must be used when administering IGIV to patients with IgAD if their anti-IgA status is unknown. A history devoid of previous blood product administration does not exclude the possibility of anti-IgA antibodies or adverse reactions. Fortunately, appropriate precautions can significantly reduce morbidity (see Treatment). Blood banks can use a simple ELISA screening approach to establish an IgAD blood donor poo
Pulmonary hypertension is a type of high blood pressure that affects the arteries in your lungs and the right side of your heart. In one form of pulmonary hypertension, tiny arteries in your lungs, called pulmonary arterioles, and capillaries become narrowed, blocked or destroyed. This makes it harder for blood to flow through your lungs, and raises pressure within your lungs' arteries. As the pressure builds, your heart's lower right chamber (right ventricle) must work harder to pump blood through your lungs, eventually causing your heart muscle to weaken and fail. Some forms of pulmonary hypertension are serious conditions that become progressively worse and are sometimes fatal. Although some forms of pulmonary hypertension aren't curable, treatment can help lessen symptoms and improve your quality of life. Pulmonary hypertension care at Mayo Clinic