This Video COPD, or chronic obstructive pulmonary (PULL-mun-ary) disease, is a progressive disease that makes it hard to breathe. "Progressive" means the disease gets worse over time. COPD can cause coughing that produces large amounts of mucus (a slimy substance), wheezing, shortness of breath, chest tightness, and other symptoms. Cigarette smoking is the leading cause of COPD. Most people who have COPD smoke or used to smoke. Long-term exposure to other lung irritants—such as air pollution, chemical fumes, or dust—also may contribute to COPD.

Dr. Berger, Medical Director of Chapel Hill Tubal Reversal Center discusses the pros and cons of tubal reversal vs. IVF with a couple wanting a baby after a tubal ligation.

What is an Aneurysm? A cerebral or intracranial aneurysm is an abnormal focal dilation of an artery in the brain that results from a weakening of the inner muscular layer (the intima) of a blood vessel wall. The vessel develops a "blister-like" dilation that can become thin and rupture without warning. The resultant bleeding into the space around the brain is called a subarachnoid hemorrhage (SAH). This kind of hemorrhage can lead to a stroke, coma, and/or death. Aneurysms are usually found at the base of the brain just inside the skull, in an area called the subarachnoid space. In fact, 90 percent of SAHs are attributed to ruptured cerebral aneurysms and the two terms are often used synonymously.

Orchidectomy and Orchidopexy in Testicular Torsion

There are several approaches to scoliosis surgery, but all use modern instrumentation systems in which hooks and screws are applied to the spine to anchor long rods. The rods are then used to reduce and hold the spine while bone that is added fuses together with existing bone.

Abscess drainage in neck

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

Sclerotherapy is a medical procedure used to eliminate varicose veins and spider veins. Sclerotherapy involves an injection of a solution (generally a salt solution) directly into the vein. The solution irritates the lining of the blood vessel, causing it to collapse and stick together and the blood to clot.

Polymyalgia rheumatica is an inflammatory disorder that causes muscle pain and stiffness, especially in the shoulders. Symptoms of polymyalgia rheumatica (pol-e-my-AL-juh rue-MAT-ih-kuh) usually begin quickly and are worse in the morning. Most people who develop polymyalgia rheumatica are older than 65. It rarely affects people under 50. You may receive symptom relief by taking anti-inflammatory drugs called corticosteroids. But relapses are common, and you'll need to visit your doctor regularly to watch for serious side effects of these drugs. Polymyalgia rheumatica is related to another inflammatory disorder called giant cell arteritis, which can cause headaches, vision difficulties, jaw pain and scalp tenderness. It's possible to have both of these conditions together.

Testicular Self Exam

Alcohol septal ablation (ASA, TASH, Sigwart procedure) is a percutaneous, minimally-invasive treatment performed by an interventional cardiologist to relieve symptoms and improve functional status in severely symptomatic patients with hypertrophic cardiomyopathy (HCM) who meet strict clinical, anatomic and physiologic ...

Imperforate Hymen

X-linked agammaglobulinemia (XLA), or Bruton agammaglobulinemia, is an inherited immunodeficiency disease caused by mutations in the gene coding for Bruton tyrosine kinase (BTK). The disease was first elucidated by Bruton in 1952, for whom the gene is named. BTK is critical to the maturation of pre–B cells to differentiating mature B cells. The BTK gene defect has been mapped to the long arm of the X chromosome at band Xq21.3 to Xq22, spanning 37.5kb with 19 exons forming 659 amino acids to complete the BTK cytosolic tyrosine kinase. A database of BTK mutations (BTKbase: Mutation registry for X-linked agammaglobulinemia) lists 544 mutation entries from 471 unrelated families showing 341 unique molecular events. No single mutation accounts for more than 3% of mutations in patients. In addition to mutations, a number of variants or polymorphisms have been found.

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

In this video I discuss sexual function for people with a spinal cord injury. The amount of feeling and function can vary drastically depending on the level and severity of the injury to the spinal cord.

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The pelvic diaphragm is composed of muscle fibers of the levator ani, the coccygeus, and associated connective tissue which span the area underneath the pelvis. The pelvic diaphragm is a muscular partition formed by the levatores ani and coccygei, with which may be included the parietal pelvic fascia on their upper and lower aspects. The pelvic floor separates the pelvic cavity above from the perineal region (including perineum) below.

The right and left levator ani lie almost horizontally in the floor of the pelvis, separated by a narrow gap that transmits the urethra, vagina, and anal canal. The levator ani is usually considered in three parts: pubococcygeus, puborectalis, and iliococcygeus. The pubococcygeus, the main part of the levator, runs backward from the body of the pubis toward the coccyx and may be damaged during parturition. Some fibers are inserted into the prostate, urethra, and vagina. The right and left puborectalis unite behind the anorectal junction to form a muscular sling . Some regard them as a part of the sphincter ani externus. The iliococcygeus, the most posterior part of the levator ani, is often poorly developed.

The coccygeus, situated behind the levator ani and frequently tendinous as much as muscular, extends from the ischial spine to the lateral margin of the sacrum and coccyx.

The pelvic cavity of the true pelvis has the pelvic floor as its inferior border (and the pelvic brim as its superior border.) The perineum has the pelvic floor as its superior border.

Some sources do not consider “pelvic floor” and “pelvic diaphragm” to be identical, with the “diaphragm” consisting of only the levator ani and coccygeus, while the “floor” also includes the perineal membrane and deep perineal pouch.

Giving Birth

A to Z in ecg arabic lesson 2