Nice surgery video

Combined Complete Total Gastrectomy with Left Hemipancreatectomy, Splenectomy, Resection of Mesocolon, D3-Lymphadenectomy for Local Advanced Gastric Cancer with Stage IV (T4N2M0).

Graphic video demonstrating the reconstruction of a facial cheek defect following the removal of a common skin cancer in a challenging location near the lower eyelid. Visit us @ www.skincancercentre.com.

ROTIGS medical device by Honolulu inventor Dr. Brad NaPier makes difficult airway intubations easier for medical professionals.

A high definition medical video showing the Laparoscopic inguinal hernia repair

Examination of Neck Swelling

Histology of Spinal Cord

Histology of Ovary

Basic Respiratory Clinical Exam Video

Surgical Glove Flip How To

Pterygium Excision with Auto Conjunctival Graft

Bilateral Laparoscopic Pyeloplasty in Children

Development and Maintenance of Bone

TEE of a giant LV thrombus as well as other, smaller thrombi in a 51 year-old man who came to the hospital complaining of chest pain. He was subsequently taken to the cardiac cath lab and was found to have clean coronary arteries. Surprisingly, he was clinically stable despite his TEE findings and an EF of 20%.

Fifth disease is a mild rash illness caused by parvovirus B19. This disease, also called erythema infectiosum, got its name because it was fifth in a list of historical classifications of common skin rash illnesses in children. It is more common in children than adults. A person usually gets sick with fifth disease within 4 to 14 days after getting infected with parvovirus B19.

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

There are many factors that will determine how quickly, or completely you recover from your meniscal tear surgery. Key elements include your age, weight, and activity demands. The older you are, the heavier you are, the longer your recovery will be. The type of surgery you had will also impact upon your recovery. In some cases we only remove the torn piece — in general you will progress faster than someone who had sutures placed to repair the meniscus tear. Whether or not arthritis was found at the time of your meniscus surgery will also significantly influence your recovery from meniscus surgery. If you have arthritis then you are missing some or all of the cartilage on the ends of the bones. Knees with arthritis are prone to being more “cranky” during the recovery process. In those cases, a knee ice compression device can provide relief of pain/swelling. Many patients note they feel better wearing a compression sleeve during recovery. People with arthritis sometimes report improvement in their symptoms with supplements like Glucosamine, Curcumin, or Hyaluronic Acid which they believe (not proven) will smooth out the surface of the joint. Many try Tart Cherry juice because of its natural anti-inflammatory properties.. In the first few months following surgery, a knee compression sleeve does actually help many feel better. Some of the variables affecting your recovery from meniscus surgery are under your surgeon’s control. We can improve your immediate response after surgery with the use of various medications we inject within the knee before the surgery. We can also block a nerve on the side of your leg which will improve your pain for 18-24 hours after surgery. Many of you will purchase a ice compression sleeve to help minimize the pain after the surgery. In general, young, healthy active people with no evidence of osteoarthritis will experience a much more rapid recovery. Typically measured in days or a few weeks. Most people are off crutches in a day, and stop taking pain medicine within a day or two. In contrast, if you are a older, heavier and have arthritis as well as a meniscus tear, then you may take longer to recover — and may not experience a “full” recovery. This group can take weeks to months to improve. To ensure a good response to surgery, we also need to look at your health before surgery. Smoking leads to an increased infection rate and poorer healing. Diabetics with poor sugar control are at higher risk for infection and delays in healing as well. Obesity is a potential problem with anesthesia, the recovery from surgery and it may lead to more rapid progression of arthritis after surgery. The better shape you are in prior to surgery can influence your recovery.

Cystinuria is a condition characterized by the buildup of the amino acid cystine, a building block of most proteins, in the kidneys and bladder. As the kidneys filter blood to create urine, cystine is normally absorbed back into the bloodstream. People with cystinuria cannot properly reabsorb cystine into their bloodstream, so the amino acid accumulates in their urine. As urine becomes more concentrated in the kidneys, the excess cystine forms crystals. Larger crystals become stones that may lodge in the kidneys or in the bladder. Sometimes cystine crystals combine with calcium molecules in the kidneys to form large stones. These crystals and stones can create blockages in the urinary tract and reduce the ability of the kidneys to eliminate waste through urine. The stones also provide sites where bacteria may cause infections.

Pulmonary function tests are a broad range of tests that measure how well the lungs take in and exhale air and how efficiently they transfer oxygen into the blood. Spirometry measures how well the lungs exhale.

Rickets is the softening and weakening of bones in children, usually because of an extreme and prolonged vitamin D deficiency. Vitamin D promotes the absorption of calcium and phosphorus from the gastrointestinal tract. A deficiency of vitamin D makes it difficult to maintain proper calcium and phosphorus levels in bones, which can cause rickets. Adding vitamin D or calcium to the diet generally corrects the bone problems associated with rickets. When rickets are due to another underlying medical problem, your child may need additional medications or other treatment. Some skeletal deformities caused by rickets may require corrective surgery.