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.

The incidence of digitalis toxicity has declined in recent years, due to decreased use of this drug along with improved technology for monitoring of drug levels and increased awareness of drug interactions. Nevertheless, cardiac glycoside toxicity continues to be a problem in the United States because of the wide use of digoxin (a preparation of digitalis) and its narrow therapeutic window. Digitalis is a plant-derived cardiac glycoside commonly used in the treatment of chronic heart failure (CHF), atrial fibrillation, and reentrant supraventricular tachycardia.[1, 2] Digoxin is the only available preparation of digitalis in the United States. (See Etiology and Epidemiology.) Cardiac glycosides are found in certain flowering plants, such as oleander and lily-of-the-valley. Indigenous people in various parts of the world have used many plant extracts containing cardiac glycosides as arrow and ordeal poisons. The ancient Egyptians used squill (Urginea maritime) as a medicine. The Romans employed it as a diuretic, heart tonic, emetic, and rat poison. Digitalis, or foxglove, was mentioned in the year 1250 in the writings of Welsh physicians. Fuchsius described it botanically 300 years later and named it Digitalis purpurea. William Withering published his classic account of foxglove and some of its medical uses in 1785, remarking upon his experience with digitalis. He recognized many of the signs of digitalis toxicity, noting, "The foxglove, when given in very large and quickly repeated doses, occasions sickness, vomiting, purging, giddiness, confused vision, objects appearing green or yellow; increased secretion of urine, slow pulses, even as low as 35 in a minute, cold sweats, convulsions, syncope, death." (See Presentation and Workup.) During the early 20th century, as a result of the work of Cushny, Mackenzie, Lewis, and others, the drug was gradually recognized as specific for treatment of atrial fibrillation. Only subsequently was the value of digitalis for treatment of CHF established. Cardiac glycosides enhance cardiac contractility and slow conduction through the atrioventricular (AV) junction by increasing vagal tone.[3] (See Etiology.) Cardiac glycoside toxicity has been known to result from ingestion of some plants, including yellow oleander (Thevetia peruviana) and foxglove, and a similar toxidrome has been associated with the use of herbal dietary supplements that contain cardiac glycosides. Digoxin is among the top 50 prescribed drugs in the United States.[4] In 2011, the American Association of Poison Control Centers reported 1601 single exposures to cardiac glycoside drugs.[5] Cardiac glycosides account for 2.6% of toxic plant exposures in the United States.[6, 7] Most of these exposures are in children.[7] (See Epidemiology.) Digoxin-specific fragment antigen-binding (Fab) antibody fragments have contributed significantly to the improved morbidity and mortality of toxic patients since their approval in 1986 by the US Food and Drug Administration (FDA). (See Prognosis, Treatment, and Medication.)

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.

In neonates, hypocalcemia is more likely to occur in infants born of diabetic or preeclamptic mothers. Hypocalcemia also may occur in infants born to mothers with hyperparathyroidism. Clinically evident hypocalcemia generally presents in milder forms and is usually the result of a chronic disease state. In emergency department patients, chronic or subacute complaints secondary to mild or moderate hypocalcemia are more likely to be a chief complaint than severe symptomatic hypocalcemia. Once laboratory results demonstrate hypocalcemia, the first question is whether the hypocalcemia is true—that is, whether it is representative of a decrease in ionized calcium. The presence of chronic diarrhea or intestinal disease (eg, Crohn disease, sprue, chronic pancreatitis) suggests the possibility of hypocalcemia due to malabsorption of calcium and/or vitamin D. The patient's past medical history should be explored for pancreatitis, anxiety disorders, renal or liver failure, gastrointestinal disorders, and hyperthyroidism or hyperparathyroidism. Previous neck surgery suggests hypoparathyroidism; a history of seizures suggests hypocalcemia secondary to anticonvulsants. The patient may have a recent history of thyroid, parathyroid, or bowel surgeries or recent neck trauma. The length of time that a disorder is present is an important clue. Hypoparathyroidism and pseudohypoparathyroidism are lifelong disorders. Instead, acute transient hypocalcemia may be associated with acute gastrointestinal illness, nutritional deficiency, or acute or chronic renal failure. In an elderly patient, a nutritional deficiency may be associated with a low intake of vitamin D. A history of alcoholism can help diagnose hypocalcemia due to magnesium deficiency, malabsorption, or chronic pancreatitis. Inquire about recent use of drugs associated with hypocalcemia, including the following: Radiocontrast Estrogen Loop diuretics Bisphosphonates Calcium supplements Antibiotics Antiepileptic drugs Cinacalcet Other considerations in the history include the following: Family history of hypocalcemia Low-calcium diet Lack of sun exposure

Hyponatremia is a condition that occurs when the level of sodium in your blood is abnormally low. Sodium is an electrolyte, and it helps regulate the amount of water that's in and around your cells. In hyponatremia, one or more factors — ranging from an underlying medical condition to drinking too much water during endurance sports — causes the sodium in your body to become diluted. When this happens, your body's water levels rise, and your cells begin to swell. This swelling can cause many health problems, from mild to life-threatening. Hyponatremia treatment is aimed at resolving the underlying condition. Depending on the cause of hyponatremia, you may simply need to cut back on how much you drink. In other cases of hyponatremia, you may need intravenous fluids and medications

Sodium levels are tightly controlled in a healthy individual by regulation of urine concentration and an intact thirst mechanism. Hypernatremia (defined as a serum sodium level >145 mEq/L) is rare in patients with preserved thirst mechanism. When hypernatremia does occur, it is associated with a high mortality rate (>50% in most studies). Given this high mortality rate, the emergency physician must be able to recognize and treat this condition. This article discusses the patients in whom hypernatremia should be suspected and how to initiate workup and administer appropriate treatment. In general, hypernatremia can be caused by derangement of the thirst response or altered behavioral response thereto (primarily psychiatric patients, and elderly patients who are institutionalized), impaired renal concentrating mechanism (diabetes insipidus [DI]) secondary to kidney pathology (nephrogenic DI) or difficulty with the neurohormonal control of this concentrating mechanism (central DI), or by losses of free water from other sources.

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.

Hyperkalemia is defined as a serum potassium concentration higher than the upper limit of the normal range; the range in infants and children is age-dependent, whereas the range for adults is approximately 3.5-5.5 mEq/L. The upper limit may be considerably higher in young or premature infants, as high as 6.5 mEq/L.[5] Degrees of hyperkalemia are defined as follows[6] : 5.5-6.0 mEq/L – Mild 6.1-7.0 mEq/L – Moderate ≥7.0 mEq/L – Severe levels higher than 7 mEq/L can lead to significant hemodynamic and neurologic consequences. levels exceeding 8.5 mEq/L can cause respiratory paralysis or cardiac arrest and can quickly be fatal. Because of a paucity of distinctive signs and symptoms, hyperkalemia can be difficult to diagnose. Indeed, it is frequently discovered as an incidental laboratory finding. The physician must be quick to consider hyperkalemia in patients who are at risk for this disease process. (See Etiology.) However, any single laboratory study demonstrating hyperkalemia must be repeated to confirm the diagnosis, especially if the patient has no changes on electrocardiography (ECG). Because hyperkalemia can lead to sudden death from cardiac arrhythmias, any suggestion of hyperkalemia requires an immediate ECG to ascertain whether ECG signs of electrolyte imbalance are present (see Workup). Continuous ECG monitoring is essential if hyperkalemia is confirmed. Other testing is directed toward uncovering the condition or conditions that led to the hyperkalemia (see Workup). The aggressiveness of therapy for hyperkalemia is directly related to the rapidity with which the condition has developed, the absolute level of serum potassium, and the evidence of toxicity. The faster the rise of the potassium level, the higher it has reached, and the greater the evidence of cardiotoxicity, the more aggressive therapy should be. In severe cases, treatment focuses on immediate stabilization of the myocardial cell membrane, rapid shifting of potassium to the intracellular space, and total body potassium elimination. In addition, all sources of exogenous potassium should be immediately discontinued. (See Treatment.)

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.

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

Top 10 Shocking Before And After Drug Use Photos

Multiple Sclerosis Multiple sclerosis (MS) affects the brain and spinal cord. Early MS symptoms include weakness, tingling, numbness, and blurred vision. Other signs are muscle stiffness, thinking problems, and urinary problems. Treatment can relieve MS symptoms and delay disease progression.

Multiple sclerosis (MS) affects the brain and spinal cord. Early MS symptoms include weakness, tingling, numbness, and blurred vision. Other signs are muscle stiffness, thinking problems, and urinary problems. Treatment can relieve MS symptoms and delay disease progression.

Brown-Séquard syndrome is an incomplete spinal cord lesion characterized by a clinical picture reflecting hemisection injury of the spinal cord, often in the cervical cord region. (See Presentation.) Patients with Brown-Séquard syndrome suffer from ipsilateral upper motor neuron paralysis and loss of proprioception, as well as contralateral loss of pain and temperature sensation. A zone of partial preservation or segmental ipsilateral lower motor neuron weakness and analgesia may be noted. Loss of ipsilateral autonomic function can result in Horner syndrome. (See Etiology, Presentation, and Workup.) As an incomplete spinal cord syndrome, the clinical presentation of Brown-Séquard syndrome may range from mild to severe neurologic deficit. (See Presentation.) Brown-Séquard–plus syndrome The pure Brown-Séquard syndrome reflecting hemisection of the cord is not often observed. A clinical picture composed of fragments of the syndrome or of the hemisection syndrome plus additional symptoms and signs is more common. These less-pure forms of the disorder are often referred to as Brown-Séquard–plus syndrome.[1] Interruption of the lateral corticospinal tracts, the lateral spinal thalamic tract, and at times the posterior columns produces a picture of a spastic, weak leg with brisk reflexes and a strong leg with loss of pain and temperature sensation. Note that spasticity and hyperactive reflexes may not be present with an acute lesion.

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

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.

Guillain-Barre (gee-YAH-buh-RAY) 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.

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.

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.

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.