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La sindrome da reflusso acido, nota anche come sindrome da reflusso gastro-esofageo (GERD), si verifica a causa della coesistenza di diversi disturbi medici e di stile di vita.

Fattori fisiologici che scatenano GERD includono l'ipotonia dello sfintere esofageo inferiore (LES) (il graduale indebolimento del LES), insieme con il flusso retrogrado del contenuto dello stomaco nell'esofago, e il livello di sensibilità del muco esofagea al contenuto riflusso.


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Carpal tunnel surgery, also called carpal tunnel release (CTR) and carpal tunnel decompression surgery, is a surgery in which the transverse carpal ligament is divided. It is a treatment for carpal tunnel syndrome and recommended when there is static (constant, not just intermittent) numbness, muscle weakness, or atrophy, and when night-splinting no longer controls intermittent symptoms of pain in the carpal tunnel. In general, milder cases can be controlled for months to years, but severe cases are unrelenting symptomatically and are likely to result in surgical treatment.

HIV is spread only in certain body fluids from a person infected with HIV. These fluids are blood, semen, pre-seminal fluids, rectal fluids, vaginal fluids, and breast milk. In the United States, HIV is spread mainly by having sex or sharing injection drug equipment, such as needles, with someone who has HIV. To reduce your risk of HIV infection, use condoms correctly every time you have vaginal, oral, or anal sex. Don’t inject drugs. If you do, use only sterile injection equipment and water and never share your equipment with others. Pre-exposure prophylaxis (PrEP) is an HIV prevention option for people who don’t have HIV but who are at high risk of becoming infected with HIV. PrEP involves taking a specific HIV medicine every day. PrEP should always be combined with other prevention options, such as condoms.

Before the angioplasty procedure begins, you will receive some pain medicine. You may also be given medicine that relaxes you, and blood thinning medicines to prevent a blood clot from forming. You will lie on a padded table. Your doctor will insert a flexible tube (catheter) through a surgical cut into an artery. Sometimes the catheter will be placed in your arm or wrist, or in your upper leg or groin area. You will be awake during the procedure. The doctor will use live x-ray pictures to carefully guide the catheter up into your heart and arteries. Dye will be injected into your body to highlight blood flow through the arteries. This helps the doctor see any blockages in the blood vessels that lead to your heart. A guide wire is moved into and across the blockage. A balloon catheter is pushed over the guide wire and into the blockage. The balloon on the end is blown up (inflated). This opens the blocked vessel and restores proper blood flow to the heart. A wire mesh tube (stent) may then be placed in this blocked area. The stent is inserted along with the balloon catheter. It expands when the balloon is inflated. The stent is left there to help keep the artery open

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.

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

Graves disease is an autoimmune disorder that leads to an overactive thyroid gland (hyperthyroidism). An autoimmune disorder is a condition that occurs when the immune system mistakenly attacks healthy tissue. Causes The thyroid gland is an important organ of the endocrine system. The gland is located at the front of the neck above where the collarbones meet. This gland releases the hormones thyroxine (T4) and triiodothyronine (T3), which control body metabolism. Controlling metabolism is important for regulating mood, weight, and mental and physical energy levels. When the body makes too much thyroid hormone, the condition is called hyperthyroidism. (An underactive thyroid leads to hypothyroidism.) Graves disease is the most common cause of hyperthyroidism. It is due to an abnormal immune system response that causes the thyroid gland to produce too much thyroid hormone. Graves disease is most common in women over age 20. But the disorder can occur at any age and can affect men as well. Symptoms Younger people may have these symptoms: Anxiety or nervousness, as well as problems sleeping Breast enlargement in men (possible) Problems concentrating Fatigue Frequent bowel movements Hair loss Heat intolerance and increased sweating Increased appetite, despite having weight loss Irregular menstrual periods in women Muscle weakness of the hips and shoulders Moodiness, including irritability and anger Rapid or irregular heartbeat Shortness of breath with activity Tremor Many people with Graves disease have problems with their eyes: The eyeballs may seem to be bulging out and may be painful. Eyes can feel irritated and be tearing. Double vision may be present. Older people may have these symptoms: Rapid or irregular heartbeat Chest pain Memory loss Weakness and fatigue

Primary infection with herpes simplex viruses (HSVs) is clinically more severe than recurrent outbreaks. However, most primary HSV-1 and HSV-2 infections are subclinical and may never be clinically diagnosed. Orolabial herpes Herpes labialis (eg, cold sores, fever blisters) is most commonly associated with HSV-1 infection. Oral lesions caused by HSV-2 have been identified, usually secondary to orogenital contact. Primary HSV-1 infection often occurs in childhood and is usually asymptomatic. Primary infection Symptoms of primary herpes labialis may include a prodrome of fever, followed by a sore throat and mouth and submandibular or cervical lymphadenopathy. In children, gingivostomatitis and odynophagia are also observed. Painful vesicles develop on the lips, the gingiva, the palate, or the tongue and are often associated with erythema and edema. The lesions ulcerate and heal within 2-3 weeks. Recurrences The disease remains dormant for a variable amount of time. HSV-1 reactivation in the trigeminal sensory ganglia leads to recurrences in the face and the oral, labial, and ocular mucosae. Pain, burning, itching, or paresthesia usually precedes recurrent vesicular lesions that eventually ulcerate or form a crust. The lesions most commonly occur in the vermillion border, and symptoms of untreated recurrences last approximately 1 week. Recurrent erythema multiforme lesions have been associated with orolabial HSV-1 recurrences. A recent study reported that HSV-1 viral shedding had a median duration of 48-60 hours from the onset of herpes labialis symptoms. They did not detect any virus beyond 96 hours of symptom onset.[7] Genital herpes HSV-2 is identified as the most common cause of herpes genitalis. However, HSV-1 has been increasingly identified as the causative agent in as many as 30% of cases of primary genital herpes infections likely secondary to orogenital contact. Recurrent genital herpes infections are almost exclusively caused by HSV-2. Primary infection Primary herpes genitalis occurs within 2 days to 2 weeks after exposure to the virus and has the most severe clinical manifestations. Symptoms of the primary episode typically last 2-3 weeks. In men, painful, erythematous, vesicular lesions that ulcerate most commonly occur on the penis, but they can also occur on the anus and the perineum. In women, primary herpes genitalis presents as vesicular/ulcerated lesions on the cervix and as painful vesicles on the external genitalia bilaterally. They can also occur on the vagina, the perineum, the buttocks, and, at times, the legs in a sacral nerve distribution. Associated symptoms include fever, malaise, edema, inguinal lymphadenopathy, dysuria, and vaginal or penile discharge. Females may also have lumbosacral radiculopathy, and as many as 25% of women with primary HSV-2 infections may have associated aseptic meningitis. Recurrences After primary infection, the virus may be latent for months to years until a recurrence is triggered. Reactivation of HSV-2 in the lumbosacral ganglia leads to recurrences below the waist. Recurrent clinical outbreaks are milder and often preceded by a prodrome of pain, itching, tingling, burning, or paresthesia. Individuals who are exposed to HSV and have asymptomatic primary infections may experience an initial clinical episode of genital herpes months to years after becoming infected. Such an episode is not as severe as a true primary outbreak. More than one half of individuals who are HSV-2 seropositive do not experience clinically apparent outbreaks. However, these individuals still have episodes of viral shedding and can transmit the virus to their sexual partners. Other HSV infections Localized or disseminated eczema herpeticum is also known as Kaposi varicelliform eruption. Caused by HSV-1, eczema herpeticum is a variant of HSV infection that commonly develops in patients with atopic dermatitis, burns, or other inflammatory skin conditions. Children are most commonly affected. Herpes whitlow, vesicular outbreaks on the hands and the digits, was most commonly due to infection with HSV-1. It usually occurred in children who sucked their thumbs and, prior to the widespread use of gloves, in dental and medical health care workers. The occurrence of herpes whitlow due to HSV-2 is increasingly recognized, probably due to digital-genital contact. Herpes gladiatorum is caused by HSV-1 and is seen as papular or vesicular eruptions on the face, arms, or torsos of athletes in sports involving close physical contact (classically wrestling). Disseminated HSV infection can occur in females who are pregnant and in individuals who are immunocompromised. These patients may present with atypical signs and symptoms of HSV, and the condition may be difficult to diagnose. Herpetic sycosis, a follicular infection with HSV, may present as a vesiculopustular eruption on the beard area. This infection often results from autoinoculation after shaving through a recurrent herpetic outbreak. Classically caused by HSV-1, there have been rare reports of relapsing beard folliculitis caused by type 2 HSV.[8] Neonatal HSV HSV-2 infection in pregnancy can have devastating effects on the fetus. Neonatal HSV usually manifests within the first 2 weeks of life and clinically ranges from localized skin, mucosal, or eye infections to encephalitis, pneumonitis, disseminated infection, and demise. Most women who deliver infants with neonatal HSV had no prior history, signs, or symptoms of HSV infection. Risk of transmission is highest in pregnant women who are seronegative for both HSV-1 and HSV-2 and acquire a new HSV infection in the third trimester of pregnancy. Factors that increase the risk of transmission from mother to baby include the type of genital infection at the time of delivery (higher risk with active primary infection), active lesions, prolonged rupture of membranes, vaginal delivery, and an absence of transplacental antibodies. The mortality rate for neonates is extremely high (>80%) if untreated.

Coronary artery bypass graft surgery (CABG) is a procedure used to treat coronary artery disease. Coronary artery disease (CAD) is the narrowing of the coronary arteries – the blood vessels that supply oxygen and nutrients to the heart muscle. CAD is caused by a build-up of fatty material within the walls of the arteries. This build-up narrows the inside of the arteries, limiting the supply of oxygen-rich blood to the heart muscle. One way to treat the blocked or narrowed arteries is to bypass the blocked portion of the coronary artery with a piece of a healthy blood vessel from elsewhere in the body. Blood vessels, or grafts, used for the bypass procedure may be pieces of a vein from the legs or an artery in the chest. An artery from the wrist may also be used. One end of the graft is attached above the blockage and the other end is attached below the blockage. Blood is routed around, or bypasses, the blockage by going through the new graft to reach the heart muscle. This is called coronary artery bypass surgery. Traditionally, to bypass the blocked coronary artery, a large incision is made in the chest and the heart is temporarily stopped so that the surgeon can perform the delicate procedure. To open the chest, the breastbone (sternum) is cut in half and spread apart. Once the heart is exposed, tubes are inserted into the heart so that the blood can be pumped through the body by a cardiopulmonary bypass machine (heart-lung machine). The bypass machine is necessary to pump blood while the heart is stopped and kept still in order for the surgeon to perform the bypass operation. While the traditional "open heart" procedure is still commonly done and often preferred in many situations, less invasive techniques have been developed to bypass blocked coronary arteries. "Off-pump" procedures, in which the heart does not have to be stopped, were developed in the 1990's. Other minimally invasive procedures, such as keyhole surgery (performed through very small incisions) and robotic procedures (performed with the aid of a moving mechanical device), may be used.

Ventricular tachycardia is a type of heart rhythm disorder (arrhythmia) in which the lower chambers of your heart (ventricles) beat very quickly because of a problem in your heart's electrical system. In ventricular tachycardia, your heart may not be able to pump enough blood to your body and lungs because the chambers are beating so fast that they don't have time to properly fill. Ventricular tachycardia may be brief — lasting for just seconds and often not causing symptoms — or it can last for much longer, and you can develop symptoms such as dizziness or lightheadedness, or you can even pass out. This condition usually occurs in people with other heart conditions, such as coronary artery disease, cardiomyopathy and some types of valvular heart disease. Ventricular tachycardia may lead to a condition in which your lower heart chambers quiver (ventricular fibrillation), which may cause your heart to stop (sudden cardiac arrest) and lead to death if not treated immediately. Ventricular tachycardia can also cause your heart to stop, especially if the heart is beating very quickly, if it's lasting for a long period, and if you have an underlying heart condition.

Atrial flutter (AFL) is a type of abnormal heart rate, or arrhythmia. It occurs when the upper chambers of your heart beat too fast. When the chambers in the top of your heart (atria) beat faster than the bottom ones (ventricles), it complicates your heart rhythm