Have you watched a surgery on a horse before?

LDL (Bad) Cholesterol LDL cholesterol is considered the “bad” cholesterol because it contributes to plaque, a thick, hard deposit that can clog arteries and make them less flexible. This condition is known as atherosclerosis. If a clot forms and blocks a narrowed artery, heart attack or stroke can result. Another condition called peripheral artery disease can develop when plaque buildup narrows an artery supplying blood to the legs. View an animation of cholesterolHDL (Good) Cholesterol HDL cholesterol is considered “good” cholesterol because it helps remove LDL cholesterol from the arteries. Experts believe HDL acts as a scavenger, carrying LDL cholesterol away from the arteries and back to the liver, where it is broken down and passed from the body. One-fourth to one-third of blood cholesterol is carried by HDL. A healthy level of HDL cholesterol may also protect against heart attack and stroke, while low levels of HDL cholesterol have been shown to increase the risk of heart disease.

Retropharyngeal abscess (RPA) produces the symptoms of sore throat, fever, neck stiffness, and stridor. RPA occurs less commonly today than in the past because of the widespread use of antibiotics for suppurative upper respiratory infections. The incidence of RPA in the United States is rising, however. Once almost exclusively a disease of children, RPA is observed with increasing frequency in adults. It poses a diagnostic challenge for the emergency physician because of its infrequent occurrence and variable presentation.

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

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.

Friedreich's ataxia is an inherited disease that damages your nervous system. The damage affects your spinal cord and the nerves that control muscle movement in your arms and legs. Symptoms usually begin between the ages of 5 and 15. The main symptom is ataxia, which means trouble coordinating movements. Specific symptoms include Difficulty walking Muscle weakness Speech problems Involuntary eye movements Scoliosis (curving of the spine to one side) Heart palpitations, from the heart disease which can happen along with Friedreich's ataxia People with Friedreich's ataxia usually need a wheelchair 15 to 20 years after symptoms first appear. In severe cases, people become incapacitated. There is no cure. You can treat symptoms with medicines, braces, surgery, and physical therapy.

How to Insert a Tampon

The menstrual cycle is the monthly series of changes a woman's body goes through in preparation for the possibility of pregnancy. Each month, one of the ovaries releases an egg — a process called ovulation. At the same time, hormonal changes prepare the uterus for pregnancy.

Vertigo is a sensation of spinning. If you have these dizzy spells, you might feel like you are spinning or that the world around you is spinning. Causes of Vertigo Vertigo is often caused by an inner ear problem. Some of the most common causes include: BPPV. These initials stand for benign paroxysmal positional vertigo. BPPV occurs when tiny calcium particles (canaliths) clump up in canals of the inner ear. The inner ear sends signals to the brain about head and body movements relative to gravity. It helps you keep your balance. BPPV can occur for no known reason and may be associated with age. Meniere's disease. This is an inner ear disorder thought to be caused by a buildup of fluid and changing pressure in the ear. It can cause episodes of vertigo along with ringing in the ears (tinnitus) and hearing loss. Vestibular neuritis or labyrinthitis. This is an inner ear problem usually related to infection (usually viral). The infection causes inflammation in the inner ear around nerves that are important for helping the body sense balance

Genital warts are soft growths that appear on the genitals. Genital warts are a sexually transmitted infection (STI) caused by certain strains of the human papillomavirus (HPV). These skin growths can cause pain, discomfort, and itching. They are especially dangerous for women because some types of HPV can also cause cancer of the cervix and vulva.

Pulmonary embolism symptoms can vary greatly, depending on how much of your lung is involved, the size of the clots, and whether you have underlying lung or heart disease. Common signs and symptoms include: Shortness of breath. This symptom typically appears suddenly and always gets worse with exertion. Chest pain. You may feel like you're having a heart attack. The pain may become worse when you breathe deeply (pleurisy), cough, eat, bend or stoop. The pain will get worse with exertion but won't go away when you rest. Cough. The cough may produce bloody or blood-streaked sputum. Other signs and symptoms that can occur with pulmonary embolism include: Leg pain or swelling, or both, usually in the calf Clammy or discolored skin (cyanosis) Fever Excessive sweating Rapid or irregular heartbeat Lightheadedness or dizziness

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Nosebleeds common. Most often they are a nuisance and not a true medical problem. But they can be both. Nosebleed care Sit upright and lean forward. By remaining upright, you reduce blood pressure in the veins of your nose. This discourages further bleeding. Sitting forward will help you avoid swallowing blood, which can irritate your stomach. Pinch your nose. Use your thumb and index finger to pinch your nostrils shut. Breathe through your mouth. Continue to pinch for five to 10 minutes. Pinching sends pressure to the bleeding point on the nasal septum and often stops the flow of blood. To prevent re-bleeding, don't pick or blow your nose and don't bend down for several hours after the bleeding episode. During this time remember to keep your head higher than the level of your heart. If re-bleeding occurs, blow out forcefully to clear your nose of blood clots and spray both sides of your nose with a decongestant nasal spray containing oxymetazoline (Afrin, Mucinex Moisture Smart, others). Pinch your nose again as described above and call your doctor. When to seek emergency care The bleeding lasts for more than 20 minutes The nosebleed follows an accident, a fall or an injury to your head, including a punch in the face that may have broken your nose

Chainsaw Accident! Lacerations, Cysts, Blackheads & Surgerys

If the artery were severed, blood would flow out unimpeded, although the artery wall would contract in an effort to stop the bleeding. After losing >30% of one's blood volume blood pressure would start dropping, and with less pressure the rate of bleeding would go down. At this stage if the blood loss wasn't replaced the person could die. Losing halve to two thirds of one's blood volume is considered to be fatal even if later on blood transfusion is attempted. One's total blood volume at 70ml/kg is estimated to be between 5 to 7 liters, so that makes a blood loss of between 2,5 to 4,7 L.

Most women are put on a 3 to 5 day antibiotic. Men might be put on an antibiotic for 7 to 14 days. While symptoms usually clear up around three days after antibiotic treatment, it can take up to five days for all the bacteria in your urinary tract to die off. It may take even longer for men.

High blood pressure is a common condition in which the long-term force of the blood against your artery walls is high enough that it may eventually cause health problems, such as heart disease. Blood pressure is determined both by the amount of blood your heart pumps and the amount of resistance to blood flow in your arteries. The more blood your heart pumps and the narrower your arteries, the higher your blood pressure. You can have high blood pressure (hypertension) for years without any symptoms. Even without symptoms, damage to blood vessels and your heart continues and can be detected. Uncontrolled high blood pressure increases your risk of serious health problems, including heart attack and stroke. High blood pressure generally develops over many years, and it affects nearly everyone eventually. Fortunately, high blood pressure can be easily detected. And once you know you have high blood pressure, you can work with your doctor to control it.

Tendon repair can be performed using: Local anesthesia (the immediate area of the surgery is pain-free) Regional anesthesia (the local and surrounding areas are pain-free) General anesthesia (the patient is asleep and pain-free) The surgeon makes a cut on the skin over the injured tendon. The damaged or torn ends of the tendon are sewn together. If the tendon has been severely injured, a tendon graft may be needed. In this case, a piece of tendon from the foot, toe, or another part of the body is often used. If needed, tendons are reattached to the surrounding tissue. The surgeon examines the area to see if there are any injuries to nerves and blood vessels. When the repair is complete, the wound is closed. If the tendon damage is too severe, the repair and reconstruction may have to be done at different times. The surgeon will perform one surgery to repair part of the injury, and then allow the hand to heal for a few weeks. Another surgery will be done later to complete the reconstruction and repair the tendon.

Traumatic penile injury can be due to multiple factors. Penile fracture, penile amputation, penetrating penile injuries, and penile soft tissue injuries are considered urologic emergencies and typically require surgical intervention. The goals of treatment for penile trauma are universal: preservation of penile length, erectile function, and maintenance of the ability to void while standing. Traumatic injury to the penis may concomitantly involve the urethra.[1, 2] Urethral injury and repair is beyond the scope of this article but details can be found in Urethral Trauma. Penile fracture Penile fracture is the traumatic rupture of the corpus cavernosum. Traumatic rupture of the penis is relatively uncommon and is considered a urologic emergency.[3] Sudden blunt trauma or abrupt lateral bending of the penis in an erect state can break the markedly thinned and stiff tunica albuginea, resulting in a fractured penis. One or both corpora may be involved, and concomitant injury to the penile urethra may occur. Urethral trauma is more common when both corpora cavernosa are injured.[4] Penile rupture can usually be diagnosed based solely on history and physical examination findings; however, in equivocal cases, diagnostic cavernosography or MRI should be performed. Concomitant urethral injury must be considered; therefore, preoperative retrograde urethrographic studies should generally be performed. See the images below.

Giant cell arteritis is an inflammation of the lining of arteries. Most often, it affects the arteries in your head, especially those in your temples. For this reason, giant cell arteritis is sometimes called temporal arteritis. Giant cell arteritis frequently causes headaches, scalp tenderness, jaw pain and vision problems. If left untreated, it can lead to stroke or blindness. Prompt treatment with corticosteroid medications usually relieves symptoms of giant cell arteritis and may prevent loss of vision. You'll likely begin to feel better within days of starting treatment. But even with treatment, relapses are common. You'll need to visit your doctor regularly for checkups and treatment of any side effects from taking corticosteroids.