Motivation for Medical Students!

This video, Rheumatoid arthritis is a chronic inflammatory disorder that can affect more than just your joints. In some people, the condition also can damage a wide variety of body systems, including the skin, eyes, lungs, heart and blood vessels. An autoimmune disorder, rheumatoid arthritis occurs when your immune system mistakenly attacks your own body's tissues. Unlike the wear-and-tear damage of osteoarthritis, rheumatoid arthritis affects the lining of your joints, causing a painful swelling that can eventually result in bone erosion and joint deformity. The inflammation associated with rheumatoid arthritis is what can damage other parts of the body as well. While new types of medications have improved treatment options dramatically, severe rheumatoid arthritis can still cause physical disabilities.

Learn a simple way to tell if you might be suffering from an undiagnosed autoimmune condition. Examples of autoimmune conditions include: • alopecia areata

A Lecture Presented to The International Congress of Pediatric Hepatology & Gastroenterology, September 2010

SEX DURING PREGNANCY & 7 Tips For A Healthy Pregnancy

A Bone scan or bone scintigraphy is a nuclear scanning test to find certain abnormalities in bone which are triggering the bone's attempts to heal. It is primarily used to help diagnose a number of conditions relating to bones, including: cancer of the bone or cancers that have spread (metastasized) to the bone, locating some sources of bone inflammation (e.g. bone pain such as lower back pain due to a fracture), the diagnosis of fractures that may not be visible in traditional X-ray images, and the detection of damage to bones due to certain infections and other problems.

Nuclear medicine bone scans are one of a number of methods of bone imaging, all of which are used to visually detect bone abnormalities. Such imaging studies include magnetic resonance imaging (MRI), X-ray computed tomography (CT) and in the case of 'bone scans' nuclear medicine. However, a nuclear bone scan is a functional test, which means it measures an aspect of bone metabolism, which most other imaging techniques cannot. The nuclear bone scan competes with the FDG-PET scan in seeing abnormal metabolism in bones, but it is considerably less expensive.

Nuclear bone scans are not to be confused with the completely different test often termed a "bone density scan," DEXA or DXA, which is a low exposure X-ray test measuring bone density to look for osteoporosis and other diseases where bones lose mass, without any bone re-building activity. The nuclear medicine scan technique is sensitive to areas of unusual bone re-building activity because the radiopharmaceutical is taken up by osteoblast cells which build bone. The technique therefore is sensitive to fractures and bone reaction to infections and bone tumors, including tumor metastases to bones, because all these pathologies trigger bone osteoblast activity. The bone scan is not sensitive to osteoporosis or multiple myeloma in bones, and therefore other techniques must be used to assess bone abnormalities from these diseases.

It involves placing a small, expandable tube called a stent in the narrowed artery. This procedure is also called carotid angioplasty and stenting. There are two carotid arteries-one on each side of the neck-that supply blood to the brain. These arteries can be narrowed and damaged by fatty deposits called plaque.

If you have placenta previa, it means that your placenta is lying unusually low in your uterus, next to or covering your cervix. The placenta is the pancake-shaped organ – normally located near the top of the uterus – that supplies your baby with nutrients through the umbilical cord.

Cisplatin is in a class of drugs known as platinum-containing compounds used to treat various types of cancers including metastatic testicular and ovarian tumors. The molecule was first discovered in 1845, but did not receive FDA approval until 1978. Today it is known as the "penicillin of cancer drugs," because it is so effective for many different cancers. There are three key players involved in Cisplatin's mechanism: (1) Cisplatin, (2) DNA (3) and an HMG Protein. Most Cisplatin enters the body through active transport, but some molecules are passively defused through the cell membrane. Once in the nucleus, Cisplatin can form an adduct with two consecutive guanine bases within a strand of DNA. The molecule loses its chlorine atoms in exchange for the nitrogen atoms of the target guanines. Cisplatin can bond more tightly with nitrogen because nitrogen balances the platinum charge more effectively than chlorine. It is this adduct-induced DNA bend that allows binding of proteins which contain the high mobility group, HMG domain. Once the protein is bound to the DNA, it inserts a wedge-like phenyl group of phenylalanine 37 into the widened minor groove created by the bend. The tightly bound HMG protein causes destacking of the nucleotide bases, resulting in the DNA helix becoming kinked. In this way, Cisplatin can be thought of as a monkey wrench in the DNA repair system. With the HMG protein bound to the DNA, the modified strand is not repaired properly and so the cell dies. The success of Cisplatin depends on its ratio of efficacy between cancerous and healthy cells.

Gleevecs mechanism of Action

Histology of Proliferative Endometrium

Strep throat is a bacterial infection that can make your throat feel sore and scratchy. Strep throat accounts for only a small portion of sore throats. If untreated, strep throat can cause complications, such as kidney inflammation or rheumatic fever. Rheumatic fever can lead to painful and inflamed joints, a specific type of rash or heart valve damage. Strep throat is most common in children, but it affects people of all ages. If you or your child has signs or symptoms of strep throat, see your doctor for prompt testing and treatment.

Superior vena cava syndrome (SVCS) is obstruction of blood flow through the superior vena cava (SVC). It is a medical emergency and most often manifests in patients with a malignant disease process within the thorax. A patient with SVCS requires immediate diagnostic evaluation and therapy.

Harvesting and prepare fat for grafting

Deuk Laser Disc Repair vs Traditional Spinal Fusion Comparison, Laser versus Fusion

Bleeding usually occurs from only one nostril. If the bleeding is heavy enough, the blood can fill up the nostril on the affected side and overflow within the nasopharynx (the area inside the nose where the two nostrils merge), spilling into the other nostril to cause bleeding from both sides. Blood can also drip back into the throat or down into the stomach, causing a person to spit or even vomit blood. Signs of excessive blood loss include dizziness, light-headedness, confusion, and fainting. Excessive blood loss from nosebleeds is rare. Additional bleeding from other parts of the body, such as bleeding gums when brushing teeth, blood in urine or bowel movements, or easy bruising may indicate an inability of the blood to clot. Additional bleeding or easy bruising can be a sign of a more significant medical problem.

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

A ventricular septal defect (VSD), a hole in the heart, is a common heart defect that's present at birth (congenital). The hole occurs in the wall that separates the heart's lower chambers (septum) and allows blood to pass from the left to the right side of the heart. The oxygen-rich blood then gets pumped back to the lungs instead of out to the body, causing the heart to work harder. A small ventricular septal defect may cause no problems, and many small VSDs close on their own. Larger VSDs need surgical repair early in life to prevent complications.

The Epley maneuver is a series of movements, normally carried out on a person by a doctor, to relieve the symptoms of BPPV. Research has found it to be an easy, safe, and effective treatment for the condition in both the long- and short-term. The Epley maneuver is sometimes called the particle repositioning maneuver or the canalith repositioning maneuver. These names are used because the maneuver involves a series of movements that help to reposition crystals in a person's ear that may cause feelings of dizziness. Repositioning the crystals helps to relieve the person's dizziness and nausea.