Anatomy of The Lower Limb Joints

Anatomy of The Anterior Thorax

Anatomy of The Superficial Dissection of The Upper and Lower Limbs

Histology of Gastric Fundus

Histology of lingual Tonsil

Histology of Eye

Female Foley Catheterization Technique

Paramedian Thoracic Epidural Anaesthesia

Chinese Complete Physical Clinical Exam

Eye Lid Tarsal Fracture Surgery

Big Bubble Technique

Laparoscopic duodenal ulcer perforation repair 2

Patient Greg Grindley communicates with host Bryant Gumbel and his wife for the first time while undergoing deep brain stimulation surgery at University Hospital's Case Medical Center in Cleveland, Ohio.
➡ Subscribe: http://bit.ly/NatGeoSubscribe

About National Geographic:
National Geographic is the world's premium destination for science, exploration, and adventure. Through their world-class scientists, photographers, journalists, and filmmakers, Nat Geo gets you closer to the stories that matter and past the edge of what's possible.

Get More National Geographic:
Official Site: http://bit.ly/NatGeoOfficialSite
Facebook: http://bit.ly/FBNatGeo
Twitter: http://bit.ly/NatGeoTwitter
Instagram: http://bit.ly/NatGeoInsta

Greg's First In-Surgery Conversation | Brain Surgery Live
https://youtu.be/zvqV_2zncNU

National Geographic
https://www.youtube.com/natgeo

Tracheotomy is a surgical procedure which consists of making an incision on the anterior aspect of the neck and opening a direct airway through an incision in the trachea (windpipe). The resulting stoma (hole), or tracheostomy, can serve independently as an airway or as a site for a tracheostomy tube to be inserted; this tube allows a person to breathe without the use of his or her nose or mouth. Both surgical and percutaneous techniques are widely used in current surgical practice. It is among the oldest described procedures.

What is Wallenberg syndrome? Wallenberg syndrome is a rare condition in which an infarction, or stroke, occurs in the lateral medulla. The lateral medulla is a part of the brain stem. Oxygenated blood doesn’t get to this part of the brain when the arteries that lead to it are blocked. A stroke can occur due to this blockage. This condition is also sometimes called lateral medullary infarction. The cause of the syndrome isn’t always clear, however.

The brachial plexus is the network of nerves that sends signals from your spine to your shoulder, arm and hand. A brachial plexus injury occurs when these nerves are stretched, compressed, or in the most serious cases, ripped apart or torn away from the spinal cord. Minor brachial plexus injuries, known as stingers or burners, are common in contact sports, such as football. Babies sometimes sustain brachial plexus injuries during birth. Other conditions, such as inflammation or tumors, may affect the brachial plexus. The most severe brachial plexus injuries usually result from auto or motorcycle accidents. Severe brachial plexus injuries can leave your arm paralyzed, with a loss of function and sensation. Surgical procedures such as nerve grafts, nerve transfers or muscle transfers can help restore function.

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

Croup refers to an infection of the upper airway, which obstructs breathing and causes a characteristic barking cough. The cough and other symptoms of croup are the result of swelling around the vocal cords (larynx), windpipe (trachea) and bronchial tubes (bronchi). When a cough forces air through this narrowed passage, the swollen vocal cords produce a noise similar to a seal barking. Likewise, taking a breath often produces a high-pitched whistling sound (stridor). Croup typically occurs in younger children. Croup usually isn't serious and most cases can be treated at home.

A disease of the immune system due to infection with HIV. HIV destroys the CD4 T lymphocytes (CD4 cells) of the immune system, leaving the body vulnerable to life-threatening infections and cancers. Acquired immunodeficiency syndrome (AIDS) is the most advanced stage of HIV infection. To be diagnosed with AIDS, a person with HIV must have an AIDS-defining condition or have a CD4 count less than 200 cells/mm³ (regardless of whether the person has an AIDS-defining condition).

Epley maneuver: Step 1 You will sit on the doctor's exam table with your legs extended in front of you. The doctor will turn your head so that it is halfway between looking straight ahead and looking directly to the side that causes the worst vertigo. Without changing your head position, the doctor will guide you back quickly so that your shoulders are on the table but your head is hanging over the edge of the table. In this position, the side of your head that is causing the worst vertigo is facing the floor. The doctor will hold you in this position for 30 seconds or until your vertigo stops. Epley maneuver: Step 2 Then, without lifting up your head, the doctor will turn your head to look at the same angle to the opposite side, so that the other side of your head is now facing the floor. The doctor will hold you in this position for 30 seconds or until your vertigo stops. Epley maneuver: Step 3 The doctor will help you roll in the same direction you are facing so that you are now lying on your side. (For example, if you are looking to your right, you will roll onto your right side.) The side that causes the worst vertigo should be facing up. The doctor will hold you in this position for another 30 seconds or until your vertigo stops. Epley maneuver: Step 4 The doctor will then help you to sit back up with your legs hanging off the table on the same side that you were facing. This maneuver is done with the assistance of a doctor or physical therapist. A single 10- to 15-minute session usually is all that is needed. When your head is firmly moved into different positions, the crystal debris (canaliths) causing vertigo will move freely and no longer cause symptoms.