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.

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Pulmonary hypertension is a type of high blood pressure that affects the arteries in your lungs and the right side of your heart. In one form of pulmonary hypertension, tiny arteries in your lungs, called pulmonary arterioles, and capillaries become narrowed, blocked or destroyed. This makes it harder for blood to flow through your lungs, and raises pressure within your lungs' arteries. As the pressure builds, your heart's lower right chamber (right ventricle) must work harder to pump blood through your lungs, eventually causing your heart muscle to weaken and fail. Some forms of pulmonary hypertension are serious conditions that become progressively worse and are sometimes fatal. Although some forms of pulmonary hypertension aren't curable, treatment can help lessen symptoms and improve your quality of life. Pulmonary hypertension care at Mayo Clinic

protecting the body from damage caused by hyperglycemia cannot be overstated. In the United States, 57.9% of diabetic patients have one or more diabetes complications, and 14.3% have three or more.1 Strict glycemic control is the primary method of reducing the development and progression of microvascular complications, such as retinopathy, nephropathy, and neuropathy. Aggressive treatment of dyslipidemia and hypertension decreases macrovascular complications.2-4 Glycemic Control There are two primary techniques available for physicians to assess the quality of a patient’s glycemic control: self-monitoring of blood glucose (SMBG) and interval measurement of hemoglobin A1c (HbA1c).

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Respiratory syncytial virus (RSV) is a virus that causes infections of the lungs and respiratory tract. It's so common that most children have been infected with the virus by age 2. Respiratory syncytial (sin-SISH-ul) virus can also infect adults. In adults and older, healthy children, the symptoms of respiratory syncytial virus are mild and typically mimic the common cold. Self-care measures are usually all that's needed to relieve any discomfort. Infection with respiratory syncytial virus can be severe in some cases, especially in premature babies and infants with underlying health conditions. RSV can also become serious in older adults, adults with heart and lung diseases, or anyone with a very weak immune system (immunocompromised).

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

An atrial septal defect (ASD) is a hole in the wall between the two upper chambers of your heart (atria). The condition is present from birth (congenital). Small atrial septal defects may close on their own during infancy or early childhood. Large and long-standing atrial septal defects can damage your heart and lungs. Small defects may never cause a problem and may be found incidentally. An adult who has had an undetected atrial septal defect for decades may have a shortened life span from heart failure or high blood pressure that affects the arteries in the lungs (pulmonary hypertension). Surgery may be necessary to repair atrial septal defects to prevent complications.

Dilated cardiomyopathy is a disease of the heart muscle, usually starting in your heart's main pumping chamber (left ventricle). The ventricle stretches and thins (dilates) and can't pump blood as well as a healthy heart can. The term "cardiomyopathy" is a general term that refers to the abnormality of the heart muscle itself. Dilated cardiomyopathy might not cause symptoms, but for some people it can be life-threatening. A common cause of heart failure — the heart's inability to supply the body with enough blood — dilated cardiomyopathy can also contribute to irregular heartbeats (arrhythmias), blood clots or sudden death. The condition affects people of all ages, including infants and children, but is most common in men ages 20 to 60.

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.

Guillain-Barre syndrome is a rare disorder in which your body's immune system attacks your nerves. Weakness and tingling in your extremities are usually the first symptoms. These sensations can quickly spread, eventually paralyzing your whole body. In its most severe form Guillain-Barre syndrome is a medical emergency. Most people with the condition must be hospitalized to receive treatment. The exact cause of Guillain-Barre syndrome is unknown. But it is often preceded by an infectious illness such as a respiratory infection or the stomach flu. There's no known cure for Guillain-Barre syndrome, but several treatments can ease symptoms and reduce the duration of the illness. Most people recover from Guillain-Barre syndrome, though some may experience lingering effects from it, such as weakness, numbness or fatigue.

The term chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) has been used to identify patients with a chronically progressive or relapsing symmetric sensorimotor disorder with cytoalbuminologic dissociation and interstitial and perivascular endoneurial infiltration by lymphocytes and macrophages. It can be considered the chronic equivalent of acute inflammatory demyelinating polyradiculoneuropathy, the most common form of Guillain-Barré syndrome. Signs and symptoms CIDP typically starts insidiously and evolves slowly, in either a slowly progressive or a relapsing manner, with partial or complete recovery between recurrences; periods of worsening and improvement usually last weeks or months. Most experts consider the necessary duration of symptoms to be greater than 8 weeks for the diagnosis of CIDP to be made. Symptoms reported include the following: Preceding infection (infrequent) Initial limb weakness, both proximal and distal Sensory symptoms (eg, tingling and numbness of hands and feet) Motor symptoms (usually predominant) In about 16% of patients, a relatively acute or subacute onset of symptoms In children, usually a more precipitous onset of symptoms Symptoms of autonomic system dysfunction (eg, orthostatic dizziness) Pertinent physical findings are limited to the nervous system, except when the condition is associated with other diseases. Such findings may include the following. Signs of cranial nerve (CN) involvement (eg, facial muscle paralysis or diplopia) Gait abnormalities Motor deficits (eg, symmetric weakness of both proximal and distal muscles in upper and lower extremities) Diminished or absent deep tendon reflexes Sensory deficits (typically in stocking-glove distribution) Impaired coordination See Clinical Presentation for more detail. Diagnosis Laboratory studies that may be helpful include the following: Cerebrospinal fluid analysis: Elevated protein levels are common (80% of patients); 10% of patients also have mild lymphocytic pleocytosis and increased gamma globulin Complete blood count (CBC), erythrocyte sedimentation rate (ESR), antinuclear antibody (ANA) level, biochemistry profile, and serum and urine immunoelectrophoresis (to exclude associated systemic disorders) In certain instances, genetic testing Other tests and procedures that may be warranted are as follows: MRI of the spine with gadolinium enhancement Electromyography (EMG) is a critical test to determine whether the disorder is truly a peripheral neuropathy and whether the neuropathy is demyelinating Peripheral (sural) nerve biopsy (see the image below): This is considered when the diagnosis is not completely clear, when other causes cannot be excluded, or when profound axonal involvement is observed on EMG; biopsy was once commonly recommended for most patients before immunosuppressive therapy, but current guidelines no longer recommend it

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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

Cystic fibrosis (CF) is a multisystem disease affecting the digestive system, sweat glands, upper and lower respiratory tracts, and the reproductive tract, but progressive lung disease continues to be the major cause of morbidity and mortality [1]. CF is characterized by abnormal transport of chloride and sodium across the respiratory epithelium, resulting in thickened, viscous airway secretions [2]. Over a highly variable time course ranging from months to decades after birth, individuals eventually develop chronic infection of the respiratory tract with a characteristic array of bacterial flora [3], leading to progressive respiratory insufficiency and eventual respiratory failure. The rate of progression varies widely, depending in part on genotype (including gene modifiers) as well as environmental factors. Registry data from CF Centers in the United States, Canada, and Europe indicate a median survival of about 41 years [4]. Females with CF appear to have higher morbidity and mortality than males [5]. This "gender gap" is modest but consistent across many populations and is hypothesized to be due to the pro-inflammatory effects of estrogens.

Low potassium (hypokalemia) refers to a lower than normal potassium level in your bloodstream. Potassium is a chemical (electrolyte) that is critical to the proper functioning of nerve and muscles cells, particularly heart muscle cells. Normally, your blood potassium level is 3.6 to 5.2 millimoles per liter (mmol/L). A very low potassium level (less than 2.5 mmol/L) can be life-threatening and requires urgent medical attention.

Why is this medication prescribed? Amiodarone is used to treat and prevent certain types of serious, life-threatening ventricular arrhythmias (a certain type of abnormal heart rhythm when other medications did not help or could not be tolerated. Amiodarone is in a class of medications called antiarrhythmics. It works by relaxing overactive heart muscles. How should this medicine be used? Amiodarone comes as a tablet to take by mouth. It is usually taken once or twice a day. You may take amiodarone either with or without food, but be sure to take it the same way each time.Follow the directions on your prescription label carefully, and ask your doctor or pharmacist to explain any part you do not understand. Take amiodarone exactly as directed. Do not take more or less of it or take it more often than prescribed by your doctor.

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)

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.

A salivary gland stone -- also called salivary duct stone -- is a calcified structure that may form inside a salivary gland or duct. It can block the flow of saliva into the mouth. The majority of stones affect the submandibular glands located at the floor of the mouth. Less commonly, the stones affect the parotid glands, located on the inside of the cheeks, or the sublingual glands, which are under the tongue. Many people with the condition have multiple stones. Salivary Gland Stone Causes and Symptoms Salivary stones form when chemicals in the saliva accumulate in the duct or gland. They mostly contain calcium. The exact cause is not known. But factors contributing to less saliva production and/or thickened saliva may be risk factors for salivary stones. These factors include: dehydration, poor eating, and use of certain medications (such as antihistamines), blood pressure drugs, psychiatric drugs, and bladder control drugs. Trauma to the salivary glands may also raise the risk for salivary stones. The stones cause no symptoms as they form, but if they reach a size that blocks the duct, saliva backs up into the gland, causing pain and swelling. You may feel the pain off and on, and it may get progressively worse. Inflammation and infection within the affected gland may follow. Salivary Gland Stones Diagnosis and Treatments If you have symptoms of a salivary gland stone, your doctor will first check for stones with a physical exam. Sometimes tests may also be ordered, such as X-ray, CT scan, or ultrasound.