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Meningococcal meningitis - causes, features, symptoms and treatment

Dialysis and kidney transplantation are treatments for severe kidney failure, also called kidney (or renal) failure, stage 5 chronic kidney disease, and end-stage kidney (or renal) disease. There are two types of dialysis: hemodialysis and peritoneal dialysis. When the kidneys are no longer working effectively, waste products, electrolytes, and fluid build up in the blood. Dialysis takes over a portion of the function of the failing kidneys to remove the fluid and waste products. Kidney transplantation can more completely take over the function of the failing kidneys.

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Mal Di Stomaco Rimedi, Bruciore All Esofago, Come Combattere L Acidita Di Stomaco

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Le cause del reflusso acido

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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Goiter treatment depends on the size of the goiter, your signs and symptoms, and the underlying cause. Your doctor may recommend: Observation. If your goiter is small and doesn't cause problems, and your thyroid is functioning normally, your doctor may suggest a wait-and-see approach. Medications. If you have hypothyroidism, thyroid hormone replacement with levothyroxine (Levoxyl, Synthroid, Tirosint) will resolve the symptoms of hypothyroidism as well as slow the release of thyroid-stimulating hormone from your pituitary gland, often decreasing the size of the goiter. For inflammation of your thyroid gland, your doctor may suggest aspirin or a corticosteroid medication to treat the inflammation. For goiters associated with hyperthyroidism, you may need medications to normalize hormone levels. Surgery. Removing all or part of your thyroid gland (total or partial thyroidectomy) is an option if you have a large goiter that is uncomfortable or causes difficulty breathing or swallowing, or in some cases, if you have a nodular goiter causing hyperthyroidism.

The objective of carotid endarterectomy (CEA) is to prevent strokes. In the United States, stroke is the third leading cause of death overall and the second leading cause of death for women.[1] Among patients suffering a stroke, 50-75% had carotid artery disease that would have been amenable to surgical treatment. Several prospective randomized trials have compared the safety and efficacy of CEA with those of medical therapy in symptomatic and asymptomatic patients. Data from these prospective trials have confirmed that CEA offers better protection from ipsilateral strokes than medical therapy alone in patients presenting with either symptomatic or asymptomatic carotid 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

Hypercalcemia is a condition in which the calcium level in your blood is above normal. Too much calcium in your blood can weaken your bones, create kidney stones, and interfere with the way your heart and brain works. Hypercalcemia most commonly results from overactive parathyroid glands. These four tiny glands are each about the size of a grain of rice and are located on or near the thyroid gland. Other causes of hypercalcemia include cancer, certain other medical disorders, some medications, and excessive use of calcium and vitamin D supplements. Signs and symptoms of hypercalcemia may range from nonexistent to severe. Treatment depends on the underlying cause.

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.

There is a strong association with obesity. In children younger than 10 years, it is associated with metabolic endocrine disorders {hypothyroidism, panhypopituitarism, hypogonadism, renal osteodystrophy, growth hormone abnormalities). SCFE is considered chronic if it has been present more than 3 weeks and acute if it has been present for 3 weeks or less. It is called "stable" if the patient can bear weight and "unstable" if the patient cannot ambulate. Unstable SCFE is associated with more complications, including avascular necrosis of the femoral head (AVN). SCFE is diagnosed by x-ray of the pelvis and bilateral hips. The underlying cause is a widened epiphyseal growth plate, due to abnormal cartilage maturation and endochondral ossification. The treatment is surgical, requiring immediate internal fixation with a single screw. Delay in treatment {> 24 hours) leads to increased AVN, SCFE progression from stable to unstable, and high risk of future degenerative arthritis. Prophylactic contralateral fixation of the unaffected hip is not routinely done in the U.S., except in patients with endocrine abnormalities.

A torn meniscus is one of the most common knee injuries. Any activity that causes you to forcefully twist or rotate your knee, especially when putting your full weight on it, can lead to a torn meniscus. Each of your knees has two menisci — C-shaped pieces of cartilage that act like a cushion between your shinbone and your thighbone. A torn meniscus causes pain, swelling and stiffness. You also might feel a block to knee motion and have trouble extending your knee fully. Conservative treatment — such as rest, ice and medication — is sometimes enough to relieve the pain of a torn meniscus and give the injury time to heal on its own. In other cases, however, a torn meniscus requires surgical repair.

During this week your baby's brain form channels and creases with the help of more tissues with greater surface area. Check out this video for detail information on 30 weeks pregnant -

My Skin Could Kill Me

Uterine rupture is usually when the scar from your previous caesarean section tears open. Though it's uncommon, you should be aware of this risk, particularly if you're thinking about giving birth vaginally next time. It's possible for your scar to gape slightly while you're pregnant (scar dehiscence).

Pancreatic cancer begins in the tissues of your pancreas — an organ in your abdomen that lies horizontally behind the lower part of your stomach. Your pancreas secretes enzymes that aid digestion and hormones that help regulate the metabolism of sugars. Pancreatic cancer often has a poor prognosis, even when diagnosed early. Pancreatic cancer typically spreads rapidly and is seldom detected in its early stages, which is a major reason why it's a leading cause of cancer death. Signs and symptoms may not appear until pancreatic cancer is quite advanced and complete surgical removal isn't possible.

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.