A carotid endarterectomy is performed in a sterile surgical suite or standard operating room. You may go home the same day or stay 1–2 nights after the procedure depending on your medical condition. You receive a local anesthetic or general anesthesia. Your vascular surgeon makes an incision at the front of your neck. After removing the plaque from the artery your vascular surgeon repairs the artery by stitching in a natural graft (formed from a piece of vein from elsewhere in your body) or a woven patch. The incision is closed

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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

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.

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

Clopidogrel keeps the platelets in your blood from coagulating (clotting) to prevent unwanted blood clots that can occur with certain heart or blood vessel conditions. Clopidogrel is used to prevent blood clots after a recent heart attack or stroke, and in people with certain disorders of the heart or blood vessels. Clopidogrel may also be used for other purposes not listed in this medication guide

Plantar warts are hard, grainy growths that usually appear on the heels or balls of your feet, areas that feel the most pressure. This pressure also may cause plantar warts to grow inward beneath a hard, thick layer of skin (callus). Plantar warts are caused by the human papillomavirus (HPV). The virus enters your body through tiny cuts, breaks or other weak spots on the bottom of your feet. Most plantar warts aren't a serious health concern and may not require treatment. But plantar warts can cause discomfort or pain. If self-care treatments for plantar warts don't work, you may want to see your doctor to have them removed.

You might not notice signs or symptoms of Hashimoto's disease at first, or you may notice a swelling at the front of your throat (goiter). Hashimoto's disease typically progresses slowly over years and causes chronic thyroid damage, leading to a drop in thyroid hormone levels in your blood. The signs and symptoms are mainly those of an underactive thyroid gland (hypothyroidism). Signs and symptoms of hypothyroidism include: Fatigue and sluggishness Increased sensitivity to cold Constipation Pale, dry skin A puffy face Hoarse voice Unexplained weight gain — occurring infrequently and rarely exceeding 10 to 20 pounds, most of which is fluid Muscle aches, tenderness and stiffness, especially in your shoulders and hips Pain and stiffness in your joints and swelling in your knees or the small joints in your hands and feet Muscle weakness, especially in your lower extremities Excessive or prolonged menstrual bleeding (menorrhagia) Depression

Thalassemia (thal-uh-SEE-me-uh) is an inherited blood disorder characterized by less hemoglobin and fewer red blood cells in your body than normal. Several types of thalassemia exist, including alpha-thalassemia, beta-thalassemia intermedia, Cooley's anemia and Mediterranean anemia. Hemoglobin is the substance in your red blood cells that allows them to carry oxygen. The low hemoglobin and fewer red blood cells of thalassemia may cause anemia, leaving you fatigued. If you have mild thalassemia, you may not need treatment. But, if you have a more severe form of thalassemia, you may need regular blood transfusions. You can also take steps on your own to cope with fatigue, such as choosing a healthy diet and exercising regularly.

Hypertensive emergencies encompass a spectrum of clinical presentations in which uncontrolled blood pressures (BPs) lead to progressive or impending end-organ dysfunction. In these conditions, the BP should be lowered aggressively over minutes to hours. Neurologic end-organ damage due to uncontrolled BP may include hypertensive encephalopathy, cerebral vascular accident/cerebral infarction, subarachnoid hemorrhage, and/or intracranial hemorrhage.[1] Cardiovascular end-organ damage may include myocardial ischemia/infarction, acute left ventricular dysfunction, acute pulmonary edema, and/or aortic dissection. Other organ systems may also be affected by uncontrolled hypertension, which may lead to acute renal failure/insufficiency, retinopathy, eclampsia, or microangiopathic hemolytic anemia.[1] With the advent of antihypertensives, the incidence of hypertensive emergencies has declined from 7% to approximately 1% of patients with hypertension.[2] In addition, the 1-year survival rate associated with this condition has increased from only 20% (prior to 1950) to a survival rate of more than 90% with appropriate medical treatment

Electrophysiology studies test the electrical activity of your heart to find where an arrhythmia (abnormal heartbeat) is coming from. These results can help you and your doctor decide whether you need medicine, a pacemaker, an implantable cardioverter defibrillator (ICD), cardiac ablation or surgery.

AFib is caused by abnormal electrical impulses in the atria, which are the upper chambers of the heart. The result is a rapid and irregular pumping of blood through the atria. These chambers fibrillate, or quiver, rapidly.

Rapid Algorithm Review Ventricular Fibrillation

ERCP is a procedure that enables your physician to examine the pancreatic and bile ducts. A bendable, lighted tube (endoscope) about the thickness of your index finger is placed through your mouth and into your stomach and first part of the small intestine (duodenum). In the duodenum a small opening is identified (ampulla) and a small plastic tube (cannula) is passed through the endoscope and into this opening. Dye (contrast material) is injected and X-rays are taken to study the ducts of the pancreas and liver.

The uterus, or womb, is an important female reproductive organ. It is the place where a baby grows when a women is pregnant. There are different types of uterine cancer. The most common type starts in the endometrium, the lining of the uterus. This type of cancer is sometimes called endometrial cancer. The symptoms of uterine cancer include Unusual vaginal bleeding or discharge Trouble urinating Pelvic pain Pain during intercourse Uterine cancer usually occurs after menopause. Being obese and taking estrogen-alone hormone replacement therapy (also called menopausal hormone therapy) also increase your risk. Treatment varies depending on your overall health, how advanced the cancer is and whether hormones affect its growth. Treatment is usually a hysterectomy, which is surgery to remove the uterus. The ovaries and fallopian tubes are also removed. Other options include hormone therapy and radiation.

Sleep apnea is a potentially serious sleep disorder in which breathing repeatedly stops and starts. You may have sleep apnea if you snore loudly, and you feel tired even after a full night's sleep. The main types of sleep apnea are: Obstructive sleep apnea, the more common form that occurs when throat muscles relax. Central sleep apnea, which occurs when your brain doesn't send proper signals to the muscles that control breathing. Complex sleep apnea syndrome, also known as treatment-emergent central sleep apnea, occurs when someone has both obstructive sleep apnea and central sleep apnea. If you think you might have any form of sleep apnea, see your doctor. Treatment can ease your symptoms and may help prevent heart problems and other complications.

Your headache symptoms can help your doctor determine its cause and the appropriate treatment. Most headaches aren't the result of a serious illness, but some may result from a life-threatening condition requiring emergency care. Headaches are generally classified by cause: Primary headaches A primary headache is caused by overactivity of or problems with pain-sensitive structures in your head. A primary headache isn't a symptom of an underlying disease. Chemical activity in your brain, the nerves or blood vessels surrounding your skull, or the muscles of your head and neck (or some combination of these factors) can play a role in primary headaches. Some people may also carry genes that make them more likely to develop such headaches. The most common primary headaches are: Cluster headache Migraine (with and without aura) Tension headache (also known as tension-type headache) Trigeminal autonomic cephalalgia (TAC), such as cluster headache and paroxysmal hemicrania A few headache patterns also are generally considered types of primary headache, but are less common. These headaches have distinct features, such as an unusual duration or pain associated with a certain activity. Although generally considered primary, each could be a symptom of an underlying disease. They include: Chronic daily headaches (for example, chronic migraine, chronic tension-type headache, or hemicranias continua) Cough headaches Exercise headaches Sex headaches Some primary headaches can be triggered by lifestyle factors, including: Alcohol, particularly red wine Certain foods, such as processed meats that contain nitrates Changes in sleep or lack of sleep Poor posture Skipped meals Stress Secondary headaches A secondary headache is a symptom of a disease that can activate the pain-sensitive nerves of the head. Any number of conditions — varying greatly in severity — may cause secondary headaches. Possible causes of secondary headaches include: Acute sinusitis Arterial tears (carotid or vertebral dissections) Blood clot (venous thrombosis) within the brain — separate from stroke Brain aneurysm (a bulge in an artery in your brain) Brain AVM (brain arteriovenous malformation) — an abnormal formation of brain blood vessels Brain tumor Carbon monoxide poisoning Chiari malformation (structural problem at the base of your skull) Concussion Dehydration Dental problems Ear infection (middle ear) Encephalitis (brain inflammation) Giant cell arteritis (inflammation of the lining of the arteries) Glaucoma (acute angle closure glaucoma) Hangovers

10 Horrifying Things Found Living Inside a Human Body

HYSTERECTOMY RECOVERY: ALL PROCEDURES ARE NOT CREATED EQUAL Too often, women are only given the option of an open hysterectomy for conditions like large fibroids or an enlarged uterus. Surgical techniques have evolved in the last decade, but across the United States, the number of women still having open hysterectomy procedures is unnecessarily staggering. Robotic procedures are becoming more common as hospitals invest nearly $2 million in the machine. While the robot does allow surgeons who are not necessarily trained in laparoscopic procedures to perform a more minimally invasive surgery, tools cannot replace skill. There is no added benefit to the patient and the surgery can cost on average up to $2,000 more than other laparoscopic options, and in some cases much higher.

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