Coarctation of the aorta (CoA[1][2] or CoAo), also called aortic narrowing, is a congenital condition whereby the aorta is narrow, usually in the area where the ductus arteriosus (ligamentum arteriosum after regression) inserts. The word “coarctation” means narrowing. Coarctations are most common in the aortic arch. The arch may be small in babies with coarctations. Other heart defects may also occur when coarctation is present, typically occurring on the left side of the heart. When a patient has a coarctation, the left ventricle has to work harder. Since the aorta is narrowed, the left ventricle must generate a much higher pressure than normal in order to force enough blood through the aorta to deliver blood to the lower part of the body. If the narrowing is severe enough, the left ventricle may not be strong enough to push blood through the coarctation, thus resulting in lack of blood to the lower half of the body. Physiologically its complete form is manifested as interrupted aortic arch

Patent ductus arteriosus (PDA) is a persistent opening between two major blood vessels leading from the heart. The opening, called the ductus arteriosus, is a normal part of a baby's circulatory system before birth that usually closes shortly after birth. If it remains open, however, it's called a patent ductus arteriosus. A small patent ductus arteriosus often doesn't cause problems and might never need treatment. However, a large patent ductus arteriosus left untreated can allow poorly oxygenated blood to flow in the wrong direction, weakening the heart muscle and causing heart failure and other complications. Treatment options for a patent ductus arteriosus include monitoring, medications and closure by cardiac catheterization or surgery.

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.

Tetralogy of Fallot (teh-TRAL-uh-jee of fuh-LOW) is a rare condition caused by a combination of four heart defects that are present at birth. These defects, which affect the structure of the heart, cause oxygen-poor blood to flow out of the heart and to the rest of the body. Infants and children with tetralogy of Fallot usually have blue-tinged skin because their blood doesn't carry enough oxygen. Tetralogy of Fallot is often diagnosed during infancy or soon after. However, tetralogy of Fallot might not be detected until later in life, depending on the severity of the defects and symptoms. With early diagnosis followed by appropriate surgical treatment, most children who have tetralogy of Fallot live relatively normal lives, though they'll need regular medical care and might have restrictions on exercise.

Respiratory syncytial virus (RSV) is a virus that causes infections of the lungs and respiratory tract. It's so common that most children have been infected with the virus by age 2. Respiratory syncytial (sin-SISH-ul) virus can also infect adults. In adults and older, healthy children, the symptoms of respiratory syncytial virus are mild and typically mimic the common cold. Self-care measures are usually all that's needed to relieve any discomfort. Infection with respiratory syncytial virus can be severe in some cases, especially in premature babies and infants with underlying health conditions. RSV can also become serious in older adults, adults with heart and lung diseases, or anyone with a very weak immune system (immunocompromised).

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.

Asplenia is the absence of spleen and/or its functions. Abnormalities of the spleen may be classified on a pattern oriented approach, based on splenic imaging.[1] These include anomalies of the following: Shape (clefts, notches, lobules) Location (wandering spleen) Number (asplenia, polysplenia) Size (splenomegaly, atrophy) Solitary lesions (cysts, lymphangiomas, hemangiomas, hamartomas) Multiple lesions (trauma, infections, neoplasms, storage disorders) Diffuse disease (infarction, heavy metal deposition, peliosis) Absence of splenic tissue can be total (congenital asplenia) or partial (hypoplastic) from birth. Loss of splenic tissue due to surgical removal may occur later in life as a result of trauma that causes rupture of the organ. The spleen may be removed in other conditions (eg, hemoglobinopathies) to improve the red cell life expectancy. Removal of the spleen may be undertaken as a result of being involved in a neoplastic processor as a staging procedure in some cancers. Occasionally, the spleen may be removed to address the sheer mass effect of a massive enlargement (such as in storage disorders), which can cause mass effects. Autosplenectomy is the process where the spleen loses its function due to multiple and repeated infarctive episodes, as in sickle hemoglobinopathies. See the image below.

Severe combined immunodeficiency (SCID) is a life-threatening syndrome of recurrent infections, diarrhea, dermatitis, and failure to thrive. It is the prototype of the primary immunodeficiency diseases and is caused by numerous molecular defects that lead to severe compromise in the number and function of T cells, B cells, and occasionally natural killer (NK) cells. Clinically, most patients present before age 3 months. Without intervention, SCID usually results in severe infection and death in children by age 2 years. A committee of experts, initially sponsored by the World Health Organization (WHO), meets every 2 years with the goal to classify the group of primary immunodeficiency diseases according to current understanding of the pathways that become defective in the immune system.[1] Eight classification groups have been determined, with SCID being one of the best studied. Over the past few decades, the diverse molecular genetic causes of SCID have been identified with progress from studies of the immune system.[2] SCID is considered a pediatric emergency because survival depends on expeditious stem cell reconstitution, usually by bone marrow transplantation (BMT). Appropriate diagnosis is essential because instituting proper treatment is lifesaving. Despite the heterogeneity in the pathogenesis of immune defects, common cutaneous manifestations and typical infections can provide clinical clues in diagnosing this pediatric emergency.[3] Skin manifestations were prevalent in primary immunodeficiency disorders studied in 128 pediatric patients in Kuwait; skin infections were the most prevalent findings, seen in 39 patients (30%), followed by dermatitis in 24 (19%).[4] Skin infections were significantly more prevalent in those with congenital defects in phagocyte number, function, or both, as well as in those with well-defined immunodeficiencies. Dermatitis was evident in all patients with hyper–immunoglobulin (Ig) E syndrome and Wiskott-Aldrich syndrome.[4] Erythroderma of infancy with diffuse alopecia was seen exclusively in patients with SCID disorders, and telangiectasia in patients with ataxia telangiectasia; and partial albinism with silvery gray hair was associated with Chediak-Higashi syndrome. With the advances in BMT and gene therapy, patients now have a better likelihood of developing a functional immune system in a previously lethal genetic disease. However, once an infant develops serious infections, intervention is rarely successful.

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

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.

DiGeorge syndrome, also called 22q11.2 deletion syndrome, is a disorder caused by a defect in chromosome 22. It results in the poor development of several body systems. Medical problems commonly associated with DiGeorge syndrome include heart defects, poor immune system function, a cleft palate, complications related to low levels of calcium in the blood, and delayed development with behavioral and emotional problems. The number and severity of symptoms associated with DiGeorge syndrome vary greatly. However, almost everyone with DiGeorge syndrome needs treatment from specialists in a variety of fields. Before the discovery of the chromosome 22 defect, the disorder was known by several names — DiGeorge syndrome, velocardiofacial syndrome, Shprintzen syndrome, CATCH22 and others. Although the term "22q11.2 deletion syndrome" is frequently used today — and is generally a more accurate description — previous names for the disorder are still used.

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Most of the time, treatment for hemorrhoids involves steps that you can take on your own, such as lifestyle modifications. But sometimes medications or surgical procedures are necessary. Medications If your hemorrhoids produce only mild discomfort, your doctor may suggest over-the-counter creams, ointments, suppositories or pads. These products contain ingredients, such as witch hazel or hydrocortisone, that can relieve pain and itching, at least temporarily. Don't use an over-the-counter cream or other product for more than a week unless directed by your doctor. These products can cause side effects, such as skin rash, inflammation and skin thinning. Minimally invasive procedures If a blood clot has formed within an external hemorrhoid, your doctor can remove the clot with a simple incision, which may provide prompt relief. For persistent bleeding or painful hemorrhoids, your doctor may recommend another minimally invasive procedure. These treatments can be done in your doctor's office or other outpatient setting. Rubber band ligation. Your doctor places one or two tiny rubber bands around the base of an internal hemorrhoid to cut off its circulation. The hemorrhoid withers and falls off within a week. This procedure — called rubber band ligation — is effective for many people. Hemorrhoid banding can be uncomfortable and may cause bleeding, which might begin two to four days after the procedure but is rarely severe. Injection (sclerotherapy). In this procedure, your doctor injects a chemical solution into the hemorrhoid tissue to shrink it. While the injection causes little or no pain, it may be less effective than rubber band ligation. Coagulation (infrared, laser or bipolar). Coagulation techniques use laser or infrared light or heat. They cause small, bleeding, internal hemorrhoids to harden and shrivel. While coagulation has few side effects, it's associated with a higher rate of hemorrhoids coming back (recurrence) than is the rubber band treatment. Surgical procedures If other procedures haven't been successful or you have large hemorrhoids, your doctor may recommend a surgical procedure. Surgery can be performed on an outpatient basis or you may need to stay in the hospital overnight. Hemorrhoid removal. During a hemorrhoidectomy, your surgeon removes excessive tissue that causes bleeding. Various techniques may be used. The surgery may be done with a local anesthetic combined with sedation, a spinal anesthetic or a general anesthetic. Hemorrhoidectomy is the most effective and complete way to treat severe or recurring hemorrhoids. Complications may include temporary difficulty emptying your bladder and urinary tract infections associated with this problem. Most people experience some pain after the procedure. Medications can relieve your pain. Soaking in a warm bath also may help. Hemorrhoid stapling. This procedure, called stapled hemorrhoidectomy or stapled hemorrhoidopexy, blocks blood flow to hemorrhoidal tissue. Stapling generally involves less pain than hemorrhoidectomy and allows an earlier return to regular activities. Compared with hemorrhoidectomy, however, stapling has been associated with a greater risk of recurrence and rectal prolapse, in which part of the rectum protrudes from the anus. Talk with your doctor about what might be the best option for you.

Migraine treatments can help stop symptoms and prevent future attacks. Many medications have been designed to treat migraines. Some drugs often used to treat other conditions also may help relieve or prevent migraines. Medications used to combat migraines fall into two broad categories: Pain-relieving medications. Also known as acute or abortive treatment, these types of drugs are taken during migraine attacks and are designed to stop symptoms. Preventive medications. These types of drugs are taken regularly, often on a daily basis, to reduce the severity or frequency of migraines. Your treatment strategy depends on the frequency and severity of your headaches, the degree of disability your headaches cause, and your other medical conditions. Some medications aren't recommended if you're pregnant or breast-feeding. Some medications aren't given to children. Your doctor can help find the right medication for you

protecting the body from damage caused by hyperglycemia cannot be overstated. In the United States, 57.9% of diabetic patients have one or more diabetes complications, and 14.3% have three or more.1 Strict glycemic control is the primary method of reducing the development and progression of microvascular complications, such as retinopathy, nephropathy, and neuropathy. Aggressive treatment of dyslipidemia and hypertension decreases macrovascular complications.2-4 Glycemic Control There are two primary techniques available for physicians to assess the quality of a patient’s glycemic control: self-monitoring of blood glucose (SMBG) and interval measurement of hemoglobin A1c (HbA1c).

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

The term subclavian steal describes retrograde blood flow in the vertebral artery associated with proximal ipsilateral subclavian artery stenosis or occlusion, usually in the setting of subclavian artery occlusion or stenosis proximal to the origin of the vertebral artery. Alternatively, innominate artery disease has also been associated with retrograde flow in the ipsilateral vertebral artery, particularly where the subclavian artery origin is involved. Subclavian steal is frequently asymptomatic and may be discovered incidentally on ultrasound or angiographic examination for other indications, or it may be prompted by a clinical examination finding of reduced unilateral upper limb pulse or blood pressure. In some cases, patients may develop upper limb ischemic symptoms due to reduced arterial flow in the setting of subclavian artery occlusion, or they may develop neurologic symptoms due to posterior circulation ischemia associated with exercise of the ipsilateral arm.[1] Treatment has traditionally consisted of open subclavian artery revascularization, typically via carotid-subclavian bypass or subclavian artery transposition, which are generally durable procedures. Newer, less invasive options include endovascular intervention with recanalization as appropriate and angioplasty and stenting if required. The clinical relevance of subclavian steal was described in 1961 by Reivich, Holling and Roberts; however, the recognition of retrograde vertebral artery flow dates back another 100 years to Harrison and Smyth. Some papers, including a previous version of this article, advocate restricting the term subclavian steal to patients with neurologic symptoms only, but this is incorrect in view of the substantial literature using this term to describe the hemodynamic scenario of retrograde vertebral flow and proximal subclavian artery disease.

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.

A pancreas transplant is a surgical procedure to place a healthy pancreas from a deceased donor into a person whose pancreas no longer functions properly. Your pancreas is an organ that lies behind the lower part of your stomach. One of its main functions is to make insulin, a hormone that regulates the absorption of sugar (glucose) into your cells. If your pancreas doesn't make enough insulin, blood sugar levels can rise to unhealthy levels, resulting in type 1 diabetes. Most pancreas transplants are done to treat type 1 diabetes. A pancreas transplant offers a potential cure for this condition. But it is typically reserved for those with serious diabetes complications, because the side effects of a pancreas transplant are significant. In some cases, pancreas transplants may also treat type 2 diabetes. Rarely, pancreas transplants may be used in the treatment of pancreatic, bile duct or other cancers. A pancreas transplant is often done in conjunction with a kidney transplant in people whose kidneys have been

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