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External cephalic version, or version, is a procedure used to turn a fetus from a breech position or side-lying (transverse) position into a head-down (vertex) position before labor begins. When successful, version makes it possible for you to try a vaginal birth.

Harvesting and prepare fat for grafting

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.

An intracranial hematoma occurs when a blood vessel ruptures within your brain or between your skull and your brain. The collection of blood (hematoma) compresses your brain tissue. An intracranial hematoma may occur because the fluid that surrounds your brain can't absorb the force of a sudden blow or a quick stop. Then your brain may slide forcefully against the inner wall of your skull and become bruised. Although some head injuries — such as one that causes only a brief lapse of consciousness (concussion) — can be minor, an intracranial hematoma is potentially life-threatening and often requires immediate treatment. An intracranial hematoma often, but not always, requires surgery to remove the blood.

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.

Inflammatory bowel disease (IBD) involves chronic inflammation of all or part of your digestive tract. IBD primarily includes ulcerative colitis and Crohn's disease. Both usually involve severe diarrhea, pain, fatigue and weight loss. IBD can be debilitating and sometimes leads to life-threatening complications. Ulcerative colitis (UL-sur-uh-tiv koe-LIE-tis) is an inflammatory bowel disease that causes long-lasting inflammation and sores (ulcers) in the innermost lining of your large intestine (colon) and rectum. Crohn's disease is an IBD that cause inflammation of the lining of your digestive tract. In Crohn's disease, inflammation often spreads deep into affected tissues. The inflammation can involve different areas of the digestive tract — the large intestine, small intestine or both. Collagenous (kuh-LAJ-uh-nus) colitis and lymphocytic colitis also are considered inflammatory bowel diseases but are usually regarded separately from classic inflammatory bowel disease.

Pathologic changes in chronic obstructive pulmonary disease (COPD) occur in the large (central) airways, the small (peripheral) bronchioles, and the lung parenchyma. Most cases of COPD are the result of exposure to noxious stimuli, most often cigarette smoke. The normal inflammatory response is amplified in persons prone to COPD development. The pathogenic mechanisms are not clear but are most likely diverse. Increased numbers of activated polymorphonuclear leukocytes and macrophages release elastases in a manner that cannot be counteracted effectively by antiproteases, resulting in lung destruction. The primary offender has been found to be human leukocyte elastase, with synergistic roles suggested for proteinase-3 and macrophage-derived matrix metalloproteinases (MMPs), cysteine proteinases, and a plasminogen activator. Additionally, increased oxidative stress caused by free radicals in cigarette smoke, the oxidants released by phagocytes, and polymorphonuclear leukocytes all may lead to apoptosis or necrosis of exposed cells. Accelerated aging and autoimmune mechanisms have also been proposed as having roles in the pathogenesis of COPD.[5, 6] Cigarette smoke causes neutrophil influx, which is required for the secretion of MMPs; this suggests, therefore, that neutrophils and macrophages are required for the development of emphysema. Studies have also shown that in addition to macrophages, T lymphocytes, particularly CD8+, play an important role in the pathogenesis of smoking-induced airflow limitation. To support the inflammation hypothesis further, a stepwise increase in alveolar inflammation has been found in surgical specimens from patients without COPD versus patients with mild or severe emphysema. Indeed, mounting evidence supports the concept that dysregulation of apoptosis and defective clearance of apoptotic cells by macrophages play a prominent role in airway inflammation, particularly in emphysema.[7] Azithromycin (Zithromax) has been shown to improve this macrophage clearance function, providing a possible future treatment modality.[8] In patients with stable COPD without known cardiovascular disease, there is a high prevalence of microalbuminuria, which is associated with hypoxemia independent of other risk factors.[9] Chronic bronchitis Mucous gland hyperplasia (as seen in the images below) is the histologic hallmark of chronic bronchitis. Airway structural changes include atrophy, focal squamous metaplasia, ciliary abnormalities, variable amounts of airway smooth muscle hyperplasia, inflammation, and bronchial wall thickening.

Bronchiectasis is an abnormal dilation of the proximal and medium-sized bronchi (>2 mm in diameter) caused by weakening or destruction of the muscular and elastic components of the bronchial walls. Affected areas may show a variety of changes, including transmural inflammation, edema, scarring, and ulceration, among other findings. Distal lung parenchyma may also be damaged secondary to persistent microbial infection and frequent postobstructive pneumonia. Bronchiectasis can be congenital but is most often acquired.[9] Congenital bronchiectasis usually affects infants and children. These cases result from developmental arrest of the bronchial tree. Acquired forms occur in adults and older children and require an infectious insult, impairment of drainage, airway obstruction, and/or a defect in host defense. The tissue is also damaged in part by the host response of neutrophilic proteases, inflammatory cytokines, nitric oxide, and oxygen radicals. This results in damage to the muscular and elastic components of the bronchial wall. Additionally, peribronchial alveolar tissue may be damaged, resulting in diffuse peribronchial fibrosis.[12] The result is abnormal bronchial dilatation with bronchial wall destruction and transmural inflammation. The most important functional finding of altered airway anatomy is severely impaired clearance of secretions from the bronchial tree. Impaired clearance of secretions causes colonization and infection with pathogenic organisms, contributing to the purulent expectoration commonly observed in patients with bronchiectasis. The result is further bronchial damage and a vicious cycle of bronchial damage, bronchial dilation, impaired clearance of secretions, recurrent infection, and more bronchial damage

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Beta blockers, also known as beta-adrenergic blocking agents, are medications that reduce your blood pressure. Beta blockers work by blocking the effects of the hormone epinephrine, also known as adrenaline. When you take beta blockers, your heart beats more slowly and with less force, thereby reducing blood pressure. Beta blockers also help blood vessels open up to improve blood flow. Examples of beta blockers Some beta blockers mainly affect your heart, while others affect both your heart and your blood vessels. Which one is best for you depends on your health and the condition being treated. Examples of oral beta blockers include: Acebutolol (Sectral) Atenolol (Tenormin) Bisoprolol (Zebeta) Metoprolol (Lopressor, Toprol-XL) Nadolol (Corgard) Nebivolol (Bystolic) Propranolol (Inderal LA, InnoPran XL)

Fainting occurs when the blood supply to your brain is momentarily inadequate, causing you to lose consciousness. This loss of consciousness is usually brief. Fainting can have no medical significance, or the cause can be a serious disorder. Therefore, treat loss of consciousness as a medical emergency until the signs and symptoms are relieved and the cause is known. Discuss recurrent fainting spells with your doctor. If you feel faint Lie down or sit down. To reduce the chance of fainting again, don't get up too quickly. Place your head between your knees if you sit down. If someone else faints Position the person on his or her back. If the person is breathing, restore blood flow to the brain by raising the person's legs above heart level — about 12 inches (30 centimeters) — if possible. Loosen belts, collars or other constrictive clothing. To reduce the chance of fainting again, don't get the person up too quickly. If the person doesn't regain consciousness within one minute, call 911 or your local emergency number. Check the person's airway to be sure it's clear. Watch for vomiting. Check for signs of circulation (breathing, coughing or movement). If absent, begin CPR. Call 911 or your local emergency number. Continue CPR until help arrives or the person responds and begins to breathe.

Adult CPR