Categories
Ailmemts & Remedies

Amyloidosis

Alternative Names: Amyloid – primary

Definition:
In medicine, amyloidosis refers to a variety of conditions in which amyloid proteins are abnormally deposited in organs and/or tissues. A protein is described as being amyloid if, due to an alteration in its secondary structure, it takes on a particular aggregated insoluble form similar to the beta-pleated sheet.  Symptoms vary widely depending upon the site of amyloid deposition. Amyloidosis may be inherited or acquired.

CLICK & SEE THE PICTURES

The collection of these abnormal proteins interferes with the normal functioning of the organ affected.

Since there are more than 20 different proteins that may form amyloid, there are also many different types of amyloidosis.

Classification of amyloid:
The modern classification of amyloid disease tends to use an abbreviation of the protein that makes the majority of deposits, prefixed with the letter A. For example amyloidosis caused by transthyretin is termed “ATTR.” Deposition patterns vary between patients but are almost always composed of just one amyloidogenic protein. Deposition can be systemic (affecting many different organ systems) or organ-specific. Many amyloidoses are inherited, due to mutations in the precursor protein. Other forms are due to different diseases causing overabundant or abnormal protein production – such as with over production of immunoglobulin light chains in multiple myeloma (termed AL amyloid), or with continuous overproduction of acute phase proteins in chronic inflammation (which can lead to AA amyloid).

Out of the approximately 60 amyloid proteins that have been identified so far,  at least 36 have been associated in some way with a human disease.

Amyloidosis is rare, being diagnosed in between one and five in every 100,000 people every year. It’s more common in older people and is also slightly more common in men than in women.

Causes:
The cause of primary amyloidosis is unknown, but the condition is related to abnormal production of antibodies by a type of immune cell called plasma cells.

The symptoms depend on the organs affected by the deposits. These organs can include the tongue, intestines, skeletal and smooth muscles, nerves, skin, ligaments, heart, liver, spleen, and kidneys.

Primary amyloidosis can result in conditions that include:

•Carpal tunnel syndrome
•Gastrointestinal reflux (GERD)
•Heart muscle damage (cardiomyopathy)
•Kidney failure
•Malabsorption
The deposits build up in the affected organs, causing them to become stiff, which decreases their ability to function.

Risk factors have not been identified. Primary amyloidosis is rare. It is similar to multiple myeloma, and is treated the same way.

Symptoms:

CLICK & SEE
•Enlarged tongue
•Fatigue
•Irregular heart rhythm
•Numbness of hands and feet
•Shortness of breath
•Skin changes
•Swallowing difficulties
•Swelling in the arms and legs
•Weak hand grip
•Weight loss

Additional symptoms that may be associated with this disease:
•Clay-colored stools
•Decreased urine output
•Diarrhea
•Hoarseness or changing voice
•Joint pain
•Other tongue problems
•Weakness

CLICK TO SEE THE STAGES

Diagnosis:
Exams and Tests
Your doctor may discover that you have an enlarged liver or spleen.

If specific organ damage is suspected, your doctor may order tests to confirm amyloidosis of that organ. For example:

•Abdominal ultrasound may reveal a swollen liver or spleen.
•An abdominal fat pad biopsy, rectal mucosa biopsy, or a bone marrow biopsy can help confirm the diagnosis.
•A heart evaluation, including an ECG,may reveal arrhythmias, abnormal heart sounds, or signs of congestive heart failure. An echocardiogram shows poor motion of the heart wall, due to a stiff heart muscle.
•A carpal tunnel syndrome evaluation may show that hand grips are weak.Nerve conduction velocity shows abnormalities.
•Kidney function tests may show signs of kidney failure or too much protein in the urine ( nephrotic syndrome).
?BUN level is increased.
?Serum creatinine is increased.
?Urinalysis shows protein, casts, or fat bodies.

This disease may also alter the results of the following tests:
•Bence-Jones protein (quantitative)
•Carpal tunnel biopsy
•Gum biopsy
•Immunoelectrophoresis – serum
•Myocardial biopsy
•Nerve biopsy
•Quantitative immunoglobulins
•Tongue biopsy
•Urine protein

Treatment:
It isn’t always easy to treat amyloidosis, and there is no treatment yet that specifically targets the amyloid depositing in the tissues. In cases where it’s secondary to another problem (AA amyloidosis), such as rheumatoid arthritis, treating that original problem may stop the progress of amyloidosis or may even reverse it.

In cases of primary amyloidosis (AL amyloidosis), chemotherapy drugs may be given to suppress production of new amyloid and cause regression of existing amyloid deposits.

In secondary amyloidosis, aggressive treatment of the underlying disease can improve symptoms and/or slow progression of disease. Complications such as heart failure, kidney failure, and other problems can sometimes be treated as necessary.

Occasionally, transplantation of a damaged organ is necessary. However, even after this has been carried out the new organ may become affected by amyloidosis.

Treatment may also be aimed at supporting the function of damaged tissues and treating complications such as heart or kidney failure.

Overall, many types of amyloidosis follow a steadily progressive course and may prove fatal within a year or two.

Prognosis :
The severity of the disease depends upon the organs affected. Heart and kidney involvement may lead to organ failure and death. Systemic involvement is associated with death within 1 to 3 years.

Possible Complications:
•Congestive heart failure
•Death
•Endocrine failure (hormonal disorder)
•Kidney failure
•Respiratory failure

Prevention : There is no known prevention.

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.

Resources:
http://www.bbc.co.uk/health/physical_health/conditions/amyloidosis1.shtml
http://www.nlm.nih.gov/medlineplus/ency/article/000533.htm
http://en.wikipedia.org/wiki/Amyloidosis

http://health.allrefer.com/pictures-images/amyloidosis-on-the-face.html

http://health.allrefer.com/health/cardiac-amyloidosis-dilated-cardiomyopathy.html

http://morningreporttgh.blogspot.com/2010/04/amyloidosis.html

http://gsm.utmck.edu/research/HICP/overview.cfm

http://www.pathologyatlas.ro/amyloidosis-kidney-pathology.php

Enhanced by Zemanta
Categories
Ailmemts & Remedies

Atrial Fibrillation

[amazon_link asins=’B012IIVDHA,0984951407,B01LWWGB70,1537345435,1496199766,1460280423,9386261952,B00C2FCY5U,B00PBC9TH2′ template=’ProductCarousel’ store=’finmeacur-20′ marketplace=’US’ link_id=’f85bbfb8-2c1f-11e7-af4e-19f9b8867423′]

Definition:
Atrial fibrillation (AF or A-fib) is the most common cardiac arrhythmia (abnormal heart rhythm) and involves the two upper chambers (atria) of the heart. Its name comes from the fibrillating (i.e. quivering) of the heart muscles of the atria, instead of a coordinated contraction. It can often be identified by taking a pulse and observing that the heartbeats don’t occur at regular intervals. However, a stronger indicator of AF is the absence of P waves on an electrocardiogram (ECG or EKG), which are normally present when there is a coordinated atrial contraction at the beginning of each heart beat. Risk increases with age, with 8% of people over 80 having AF.

CLICK & SEE THE PICTURES

 

In AF, the normal electrical impulses that are generated by the sinoatrial node are overwhelmed by disorganized electrical impulses that originate in the atria and pulmonary veins, leading to conduction of irregular impulses to the ventricles that generate the heartbeat. The result is an irregular heartbeat which may occur in episodes lasting from minutes to weeks, or it could occur all the time for years. The natural tendency of AF is to become a chronic condition. Chronic AF leads to a small increase in the risk of death.

Atrial fibrillation is often asymptomatic, and is not in itself generally life-threatening, but may result in palpitations, fainting, chest pain, or congestive heart failure. People with AF usually have a significantly increased risk of stroke (up to 7 times that of the general population). Stroke risk increases during AF because blood may pool and form clots in the poorly contracting atria and especially in the left atrial appendage (LAA).[4] The level of increased risk of stroke depends on the number of additional risk factors. If a person with AF has none, the risk of stroke is similar to that of the general population. However, many people with AF do have additional risk factors and AF is a leading cause of stroke.

Atrial fibrillation may be treated with medications which either slow the heart rate or revert the heart rhythm back to normal. Synchronized electrical cardioversion may also be used to convert AF to a normal heart rhythm. Surgical and catheter-based therapies may also be used to prevent recurrence of AF in certain individuals. People with AF are often given anticoagulants such as warfarin to protect them from stroke.

Classification: The American College of Cardiology (ACC), American Heart Association (AHA), and the European Society of Cardiology (ESC) recommend in their guidelines the following classification system based on simplicity and clinical relevance.

AF Category…………… Defining Characteristics
First detected ……………….  only one diagnosed episode
Paroxysmal…………………..recurrent episodes that self-terminate in less than 7 days
Persistent……………………….recurrent episodes that last more than 7 days
Permanent……………………..an ongoing long-term episode

All atrial fibrillation patients are initially in the category called first detected AF. These patients may or may not have had previous undetected episodes. If a first detected episode self-terminates in less than 7 days and then another episode begins later on, the case has moved into the category of paroxysmal AF. Although patients in this category have episodes lasting up to 7 days, in most cases of paroxysmal AF the episodes will self-terminate in less than 24 hours. If instead the episode lasts for more than 7 days, it is unlikely to self-terminate and it is called persistent AF. In this case, the episode may be terminated by cardioversion. If cardioversion is unsuccessful or it is not attempted, and the episode is ongoing for a long time (e.g. a year or more), the patient’s AF is called permanent.

Episodes that last less than 30 seconds are not considered in this classification system. Also, this system does not apply to cases where the AF is a secondary condition that occurs in the setting of a primary condition that may be the cause of the AF.

Using this classification system, it’s not always clear what an AF case should be called. For example, a case may fit into the paroxysmal AF category some of the time, while other times it may have the characteristics of persistent AF. One may be able to decide which category is more appropriate by determining which one occurs most often in the case under consideration.

In addition to the above four AF categories, which are mainly defined by episode timing and termination, the ACC/AHA/ESC guidelines describe additional AF categories in terms of other characteristics of the patient.

#Lone atrial fibrillation (LAF) – absence of clinical or echocardiographic findings of other cardiovascular disease (including hypertension), related pulmonary disease, or cardiac abnormalities such as enlargement of the left atrium, and age under 60 years

#Nonvalvular AF – absence of rheumatic mitral valve disease, a prosthetic heart valve, or mitral valve repair

#Secondary AF – occurs in the setting of a primary condition which may be the cause of the AF, such as acute myocardial infarction, cardiac surgery, pericarditis, myocarditis, hyperthyroidism, pulmonary embolism, pneumonia, or other acute pulmonary disease

Although atrial fibrillation itself usually isn’t life-threatening, it is a medical emergency. It can lead to complications. Treatments for atrial fibrillation may include medications and other interventions to try to alter the heart’s electrical system.

Symptoms:
A heart in atrial fibrillation doesn’t beat efficiently. It may not be able to pump enough blood out to your body with each heartbeat.

Some people with atrial fibrillation have no symptoms and are unaware of their condition until it’s discovered during a physical examination. Those who do have atrial fibrillation symptoms may experience:

#Palpitations, which are sensations of a racing, uncomfortable, irregular heartbeat or a flopping in your chest
#Decreased blood pressure
#Weakness
#Lightheadedness
#Confusion
#Shortness of breath
#Chest pain

Atrial fibrillation may be:

#Occasional. In this case it’s called paroxysmal (par-ok-SIZ-mul) atrial fibrillation. You may have symptoms that come and go, lasting for a few minutes to hours and then stopping on their own.
#Chronic. With chronic atrial fibrillation, symptoms may last until they’re treated.

Time to see a doctor:-
If you have any symptoms of atrial fibrillation, make an appointment with your doctor. Your doctor should be able to tell you if your symptoms are caused by atrial fibrillation or another heart arrhythmia.

If you have chest pain, seek emergency medical assistance immediately. Chest pain could signal that you’re having a heart attack.

Causes:
To pump blood, your heart muscles must contract and relax in a coordinated rhythm. Contraction and relaxation are controlled by electrical signals that travel through your heart muscle.

Your heart consists of four chambers — two upper chambers (atria) and two lower chambers (ventricles). Within the upper right chamber of your heart (right atrium) is a group of cells called the sinus node. This is your heart’s natural pacemaker. The sinus node produces the impulse that starts each heartbeat.

Normally, the impulse travels first through the atria and then through a connecting pathway between the upper and lower chambers of your heart called the atrioventricular (AV) node. As the signal passes through the atria, they contract, pumping blood from your atria into the ventricles below. As the signal passes through the AV node to the ventricles, the ventricles contract, pumping blood out to your body.

.Sinus rhythm.

..Atrial fibrillation

In atrial fibrillation, the upper chambers of your heart (atria) experience chaotic electrical signals. As a result, they quiver. The AV node — the electrical connection between the atria and the ventricles — is overloaded with impulses trying to get through to the ventricles. The ventricles also beat rapidly, but not as rapidly as the atria. The reason is that the AV node is like a highway on-ramp — only so many cars can get on at one time.

The result is a fast and irregular heart rhythm. The heart rate in atrial fibrillation may range from 100 to 175 beats a minute. The normal range for a heart rate is 60 to 100 beats a minute.

Possible causes of atrial fibrillation :-

Abnormalities or damages to the heart’s structure are the most common cause of atrial fibrillation. Possible causes of atrial fibrillation include:

#High blood pressure
#Heart attacks
#Abnormal heart valves
#Congenital heart defects
#An overactive thyroid or other metabolic imbalance
#Exposure to stimulants such as medications, caffeine or tobacco, or to alcohol
#Sick sinus syndrome — improper functioning of the heart’s natural pacemaker
#Emphysema or other lung diseases
#Previous heart surgery
#Viral infections
#Stress due to pneumonia, surgery or other illnesses
#Sleep apnea
However, some people who have atrial fibrillation don’t have any heart defects or damage, a condition called lone atrial fibrillation. In lone atrial fibrillation, the cause is often unclear, and serious complications are rare.

Atrial flutter :
Atrial flutter is similar to atrial fibrillation, but slower. If you have atrial flutter, the abnormal heart rhythm in your atria is more organized and less chaotic than the abnormal patterns common with atrial fibrillation. Sometimes you may have atrial flutter that develops into atrial fibrillation and vice versa. The symptoms, causes and risk factors of atrial flutter are similar to those of atrial fibrillation. For example, strokes are a common concern in someone with atrial flutter. As with atrial fibrillation, atrial flutter is usually not life-threatening when it’s properly treated.

Risk Factors:-

Risk factors for atrial fibrillation include:

#Age. The older you are, the greater your risk of developing atrial fibrillation.
#Heart disease. Anyone with heart disease, including valve problems, history of heart attack and heart surgery, has an increased risk of atrial fibrillation.
#High blood pressure. Having high blood pressure, especially if it’s not well controlled with lifestyle changes or medications, can increase your risk of atrial fibrillation.
#Other chronic conditions. People with thyroid problems, sleep apnea and other medical problems have an increased risk of atrial fibrillation.
#Drinking alcohol. For some people, drinking alcohol can trigger an episode of atrial fibrillation. Binge drinking — having five drinks in two hours for men, or four drinks for women — may put you at higher risk.
#Family history. An increased risk of atrial fibrillation runs in some families.

Complications:-

Clots and stroke :
One of the most common complications with atrial fibrillation is the formation of blood clots in the heart. As the blood in the upper chambers of the heart (atria) of a patient with atrial fibrillation does not flow out in a normal manner and is very turbulent, there is a greater likelihood of blood clots forming. The clots may then find their way into the lower chambers of the heart (ventricles) and eventually end up in the lungs or in the general circulation. Clots in the general circulation may eventually block arteries in the brain, causing a stroke.

A patient with atrial fibrillation is twice as likely to develop a stroke compared to other people. 5% of patients with atrial fibrillation get a stroke each year. The risk is even greater the older the patient is. The following factors raise the risk of stroke even more for patients with atrial fibrillation:

#Hypertension (high blood pressure)
#Diabetes
#Heart failure
#A history of blood clots (embolism)

Strokes may be severe and can cause paralysis of part of the body, speech problems, and even death.

Heart failure:
If the atrial fibrillation is not controlled the heart is likely to get weaker. This may lead to heart failure. Heart failure is when the heart does not pump blood around the body efficiently or properly. The patient’s left side, right side, or even both sides of the body can be affected.

Alzheimer’s disease:
There is a strong relationship between atrial fibrillation and the development of Alzheimer’s disease, according to researchers at Researchers at Intermountain Medical Center in Salt Lake City.

Diagnosis:-
The evaluation of atrial fibrillation involves diagnosis, determination of the etiology of the arrhythmia, and classification of the arrhythmia. A minimal evaluation should be performed in all individuals with AF. This includes a history and physical examination, ECG, transthoracic echocardiogram, and routine bloodwork. Certain individuals may benefit from an extended evaluation which may include an evaluation of the heart rate response to exercise, exercise stress testing, a chest x-ray, trans-esophageal echocardiography, and other studies.

Screening
Screening for atrial fibrillation is not generally performed, although a study of routine pulse checks or ECGs during routine office visits found that the annual rate of detection of AF in elderly patients improved from 1.04% to 1.63%; selection of patients for prophylactic anticoagulation would improve stroke risk in that age category.[9]

Routine primary care visit
This estimated sensitivity of the routine primary care visit is 64%. This low result probably reflects the pulse not being checked routinely or carefully.

Minimal evaluation
The minimal evaluation of atrial fibrillation should generally be performed in all individuals with AF. The goal of this evaluation is to determine the general treatment regimen for the individual. If results of the general evaluation warrant it, further studies may be then performed.

History and physical examination
The history of the individual’s atrial fibrillation episodes is probably the most important part of the evaluation. Distinctions should be made between those who are entirely asymptomatic when they are in AF (in which case the AF is found as an incidental finding on an ECG or physical examination) and those who have gross and obvious symptoms due to AF and can pinpoint whenever they go into AF or revert to sinus rhythm.

Routine bloodwork
While many cases of AF have no definite cause, it may be the result of various other problems (see below). Hence, renal function and electrolytes are routinely determined, as well as thyroid-stimulating hormone (commonly suppressed in hyperthyroidism and of relevance if amiodarone is administered for treatment) and a blood count.

In acute-onset AF associated with chest pain, cardiac troponins or other markers of damage to the heart muscle may be ordered. Coagulation studies (INR/aPTT) are usually performed, as anticoagulant medication may be commenced

Electrocardiogram
Atrial fibrillation is diagnosed on an electrocardiogram (ECG), an investigation performed routinely whenever an irregular heart beat is suspected. Characteristic findings are the absence of P waves, with unorganized electrical activity in their place, and irregular R-R intervals due to irregular conduction of impulses to the ventricles.

When ECGs are used for screening, the SAFE trial found that electronic software, primary care physicians and the combination of the two had the following sensitivities and specificities:

#Interpreted by software: sensitivity = 83%, specificity = 99%
#Interpreted by a primary care physician: sensitivity = 80%, specificity = 92%
#Interpreted by a primary care physician with software: sensitivity = 92%, specificity = 91%

If paroxysmal AF is suspected but an ECG during an office visit only shows a regular rhythm, AF episodes may be detected and documented with the use of ambulatory Holter monitoring (e.g. for a day). If the episodes are too infrequent to be detected by Holter monitoring with reasonable probability, then the patient can be monitored for longer periods (e.g. a month) with an ambulatory event monitor.

Echocardiography.
A non-invasive transthoracic echocardiogram (TTE) is generally performed in newly diagnosed AF, as well as if there is a major change in the patient’s clinical state. This ultrasound-based scan of the heart may help identify valvular heart disease (which may greatly increase the risk of stroke), left and right atrial size (which indicates likelihood that AF may become permanent), left ventricular size and function, peak right ventricular pressure (pulmonary hypertension), presence of left ventricular hypertrophy and pericardial disease.

Significant enlargement of both the left and right atria is associated with long-standing atrial fibrillation and, if noted at the initial presentation of atrial fibrillation, suggests that the atrial fibrillation is likely to be of a longer duration than the individual’s symptoms.

Extended evaluation
An extended evaluation is generally not necessary in most individuals with atrial fibrillation, and is only performed if abnormalities are noted in the limited evaluation, if a reversible cause of the atrial fibrillation is suggested, or if further evaluation may change the treatment course.

Chest X-ray
A chest X-ray is generally only performed if a pulmonary cause of atrial fibrillation is suggested, or if other cardiac conditions are suspected (particularly congestive heart failure.) This may reveal an underlying problem in the lungs or the blood vessels in the chest.  In particular, if an underlying pneumonia is suggested, then treatment of the pneumonia may cause the atrial fibrillation to terminate on its own.

Transesophageal echocardiogram
A normal echocardiography (transthoracic or TTE) has a low sensitivity for identifying thrombi (blood clots) in the heart. If this is suspected – e.g. when planning urgent electrical cardioversion – a transesophageal echocardiogram (TEE) is preferred.

The TEE has much better visualization of the left atrial appendage than transthoracic echocardiography. This structure, located in the left atrium, is the place where thrombus is formed in more than 90% of cases in non-valvular (or non-rheumatic) atrial fibrillation or flutter. TEE has a high sensitivity for locating thrombus in this area   and can also detect sluggish bloodflow in this area that is suggestive of thrombus formation.

If no thrombus is seen on TEE, the incidence of stroke, (immediately after cardioversion is performed), is very low.

Ambulatory holter monitoring
A Holter monitor is a wearable ambulatory heart monitor that continuously monitors the heart rate and heart rhythm for a short duration, typically 24 hours. In individuals with symptoms of significant shortness of breath with exertion or palpitations on a regular basis, a holter monitor may be of benefit to determine if rapid heart rates (or unusually slow heart rates) during atrial fibrillation are the cause of the symptoms.

Exercise stress testing
Some individuals with atrial fibrillation do well with normal activity but develop shortness of breath with exertion. It may be unclear if the shortness of breath is due to a blunted heart rate response to exertion due to excessive AV node blocking agents, a very rapid heart rate during exertion, or due to other underlying conditions such as chronic lung disease or coronary ischemia. An exercise stress test will evaluate the individual’s heart rate response to exertion and determine if the AV node blocking agents are contributing to the symptoms.

Treatments:-
In some people, a specific event or an underlying condition, such as a thyroid disorder, may trigger atrial fibrillation. If the condition that triggered your atrial fibrillation can be treated, you might not have any more heart rhythm problems — or at least not for quite some time. If your symptoms are bothersome or if this is your first episode of atrial fibrillation, your doctor may attempt to reset the rhythm

The treatment option best for you will depend on how long you’ve had atrial fibrillation, how bothersome your symptoms are and the underlying cause of your atrial fibrillation. Generally, the goals of treating atrial fibrillation are to:

#Reset the rhythm or control the rate
#Prevent blood clots
The strategy you and your doctor choose depends on many factors, including whether you have other problems with your heart and if you’re able to take medications that can control your heart rhythm. In some cases, you may need a more invasive treatment, such as surgery or medical procedures using catheters.

Resetting your heart’s rhythm
Ideally, to treat atrial fibrillation, the heart rate and rhythm are reset to normal. To correct your condition, doctors may be able to reset your heart to its regular rhythm (sinus rhythm) using a procedure called cardioversion, depending on the underlying cause of atrial fibrillation and how long you’ve had it.

Cardioversion can be done in two ways:

#Cardioversion with drugs. This form of cardioversion uses medications called anti-arrhythmics to help restore normal sinus rhythm. Depending on your heart condition, your doctor may recommend trying intravenous or oral medications to return your heart to normal rhythm. This is often done in the hospital with continuous monitoring of your heart rate. If your heart rhythm returns to normal, your doctor often will prescribe the same anti-arrhythmic or a similar one to try to prevent more spells of atrial fibrillation.
#Electrical cardioversion. In this brief procedure, an electrical shock is delivered to your heart through paddles or patches placed on your chest. The shock stops your heart’s electrical activity momentarily. When your heart begins again, the hope is that it resumes its normal rhythm. The procedure is performed during anesthesia.
Before cardioversion, you may be given a blood-thinning medication, such as warfarin (Coumadin), for several weeks to reduce the risk of blood clots and stroke. Unless the episode of atrial fibrillation lasted less than 24 hours, you’ll need to take warfarin for at least four to six weeks after cardioversion to prevent a blood clot from forming even after your heart is back in normal rhythm. Warfarin is a powerful medication that can have dangerous side effects if not taken exactly as directed by your doctor. If you have any concerns about taking warfarin, talk to your doctor.

Or, instead of taking warfarin, you may have a test called transesophageal echocardiography — which can tell your doctor if you have any heart blood clots — just before cardioversion. In transesophageal echocardiography, a tube is passed down your esophagus and detailed ultrasound images are made of your heart. You’ll be sedated during the test.

Maintaining a normal heart rhythm
After electrical cardioversion, anti-arrhythmic medications often are prescribed to help prevent future episodes of atrial fibrillation. Commonly used medications include:

#Amiodarone (Cordarone, Pacerone)
#Propafenone (Rythmol)
#Sotalol (Betapace)
#Dofetilide (Tikosyn)
Although these drugs can help maintain a normal heart rhythm in many people, they can cause side effects, including:

#Nausea
#Dizziness
#Fatigue
Rarely, they may cause ventricular arrhythmias — life-threatening rhythm disturbances originating in the heart’s lower chambers. These medications may be needed indefinitely. Even with medications, the chance of another episode of atrial fibrillation is high.

Heart rate control
Sometimes atrial fibrillation can’t be converted to a normal heart rhythm. Then the goal is to slow the heart rate to between 60 and 100 beats a minute (rate control). Heart rate control can be achieved two ways:

#Medications. Traditionally, doctors have prescribed the medication digoxin (Lanoxin). It can control heart rate at rest, but not as well during activity. Most people require additional or alternative medications, such as calcium channel blockers or beta blockers.
#Atrioventricular (AV) node ablation. If medications don’t work, or you have side effects, AV node ablation may be another option. The procedure involves applying radio frequency energy to the pathway connecting the upper and lower chambers of your heart (AV node) through a long, thin tube (catheter) to destroy this small area of tissue.

The procedure prevents the atria from sending electrical impulses to the ventricles. The atria continue to fibrillate, though, and anticoagulant medication is still required. A pacemaker is then implanted to establish a normal rhythm. After AV node ablation, you’ll need to continue to take blood-thinning medications to reduce the risk of stroke, because your heart rhythm is still atrial fibrillation.

Other surgical and catheter procedures
Sometimes medications or cardioversion to control atrial fibrillation doesn’t work. In those cases, your doctor may recommend a procedure to destroy the area of heart tissue that’s causing the erratic electrical signals and restore your heart to a normal rhythm. These options can include:

#Radiofrequency catheter ablation. In many people who have atrial fibrillation and an otherwise normal heart, atrial fibrillation is caused by rapidly discharging triggers, or “hot spots.” These hot spots are like abnormal pacemaker cells that fire so rapidly that the upper chambers of your heart quiver instead of beating efficiently.

Radiofrequency energy directed to these hot spots through a catheter inserted in an artery near your collarbone or leg may be used to destroy these hot spots, scarring the tissue so the erratic electrical signals are normalized. This corrects the arrhythmia without the need for medications or implantable devices. In some cases, other types of catheters that can freeze the heart tissue (cryotherapy) are used.

#Surgical maze procedure. The maze procedure is often done during an open-heart surgery. Using a scalpel, doctors create several precise incisions in the upper chambers of your heart to create a pattern of scar tissue. Because scar tissue doesn’t carry electricity, it interferes with stray electrical impulses that cause atrial fibrillation. Radiofrequency or cryotherapy can also be used to create the scars, and there are several variations of the surgical maze technique. The procedure has a high success rate, but because it usually requires open-heart surgery, it’s generally reserved for people who don’t respond to other treatments or when it can be done during other necessary heart surgery, such as coronary artery bypass surgery or heart valve repair. Some people need a pacemaker implanted after the procedure.

Preventing blood clots
Most people who have atrial fibrillation or who are undergoing certain treatments for atrial fibrillation are at especially high risk of blood clots that can lead to stroke. The risk is even higher if other heart disease is present along with atrial fibrillation. Your doctor may prescribe blood-thinning medications (anticoagulants) such as warfarin (Coumadin) in addition to medications designed to treat your irregular heartbeat. Many people have spells of atrial fibrillation and don’t even know it — so you may need lifelong anticoagulants even after your rhythm has been restored to normal. If you’re prescribed warfarin, carefully follow your doctor’s instructions on taking it. Warfarin is a powerful medication that can have dangerous side effects.

Change of Lifestyle :

You may need to make lifestyle changes that improve the overall health of your heart, especially to prevent or treat conditions such as high blood pressure. Your doctor may suggest that you:

#Eat heart-healthy foods and avoid Junk or Fast food
#Reduce your salt intake, which can help lower blood pressure
#Increase your physical activity
#Quit smoking
#Pratice regular Exercise Or walk for about 45 minutes daily

Avoid drinking more than one drink of alcohol for women or more than two drinks for men a day.

Prevention:-
There are some things you can do to try to prevent recurrent spells of atrial fibrillation. You may need to reduce or eliminate caffeinated and alcoholic beverages from your diet, because they can sometimes trigger an episode of atrial fibrillation. It’s also important to be careful when taking over-the-counter (OTC) medications. Some, such as cold medicines containing pseudoephedrine, contain stimulants that can trigger atrial fibrillation. Also, some OTC medications can have dangerous interactions with anti-arrhythmic medications.

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.

Resources:
http://en.wikipedia.org/wiki/Atrial_fibrillation
http://www.mayoclinic.com/health/atrial-fibrillation/DS00291
http://www.medicalnewstoday.com/info/atrial-fibrillation/

Reblog this post [with Zemanta]
Categories
Herbs & Plants

Desert Rose

[amazon_link asins=’B001PUHFF2,B000RKBE4O,B000W21FZU,B00KS2TDBM,B01L6YLKKM,B01AMMXBTC’ template=’ProductCarousel’ store=’finmeacur-20′ marketplace=’US’ link_id=’a64b0976-fdcc-11e6-ba43-9dd5581dfe0b’]

Botanical Name:Adenium obesum
Family: Apocynaceae
Synonyms:  Adenium somalense Balf.f. (1888), Adenium socotranum Vierh.
Common Name:Sabi Star, Kudu or Desert-rose.Due to its resemblance to plumeria, and the fact that it was introduced to the Philippines from Bangkok, Thailand, the plant was also called as Bangkok kalachuchi in the Philippines.
Kingdom: Plantae
Order: Gentianales
Genus: Adenium
Species: A. obesum

Habitat:It is native to tropical and subtropical eastern and southern Africa and Arabia.(Eastern Africa to southern Arabia)

Description:
Succulent shrub or small tree, up to 4(–6) m tall, sometimes with a fleshy taproot; stem swollen at base up to 1(–2) m in diameter; bark pale greyish-green, grey or brown, smooth, with sticky, clear or white latex; branchlets glabrescent, pubescent at apex. Leaves arranged spirally, clustered at the end of branchlets, simple; stipules minute or absent; petiole up to 4 mm long; blade linear to obovate, 3–12(–17) cm × 0.2–6 cm, base cuneate, apex acute to rounded or emarginate, entire, slightly glaucous, dull green or pale green, leathery, pinnately veined with distinct or indistinct lateral veins. Inflorescence a more or less dense terminal cyme; bracts linear to narrowly oblong, 3–8 mm long, acuminate, pubescent. Flowers bisexual, regular, 5-merous, showy, usually appearing before the leaves; pedicel 5–9 mm long; sepals narrowly oblong to narrowly ovate, 6–12 mm long, hairy; corolla with funnel-shaped tube 2–4.5 cm × 0. 9–1.7 cm, reddish-pink to white suffused with pink, sometimes red-striped inside the throat, hairy to glabrous outside, glandular hairy on main veins inside, lobes 1–3 cm × 0.5–2.5 cm, spreading, pale pink to red with darker margins; stamens inserted near base of corolla tube, included or exserted, anthers forming a cone covering the pistil, base sagittate, 5–7 mm long, with long apical appendices; ovary superior, composed of 2 free carpels, glabrous, styles fused, slender, with well-developed clavuncula. Fruit consisting of 2 linear-oblong follicles, coherent at the base, 11–22 cm long, tapering at both ends, recurved, grey to pale grey-brown, opening by a longitudinal slit, many-seeded. Seeds linear-oblong, 10–14 mm long, pale brown, slightly rough, with tufts of long dirty white hairs at both ends.

CLICK & SEE THE PICTURES

Adenium is a genus of flowering plants in the family Apocynaceae, containing a single species, Adenium obesum, also known as Sabi Star, Kudu or Desert-rose.
It is an evergreen succulent shrub in tropical climates and semi-deciduous to deciduous in colder climates, is also dependent on the subspecies or cultivar. Growing to 1–3 m in height, with pachycaul stems and a stout, swollen basal caudex. The leaves are spirally arranged, clustered toward the tips of the shoots, simple entire, leathery in texture, 5–15 cm long and 1–8 cm broad. The flowers are tubular, 2–5 cm long, with the outer portion 4–6 cm diameter with five petals, resembling those of other related genera such as Plumeria and Nerium. The flowers tend to red and pink, often with a whitish blush outward of the throat.Classification


Cultivation and uses

Adenium is a popular houseplant in temperate regions. It requires a sunny location and a minimum indoor temperature in winter of 10 °C. It thrives on a xeric watering regime as required by cacti. Adenium is typically propagated by seed or stem cuttings. The numerous hybrids are propagated mainly by grafting onto seedling rootstock. While plants grown from seed are more likely to have the swollen caudex at a young age, with time many cutting-grown plants cannot be distinguished from seedlings.

The plant exudes a highly toxic sap which is used by some peoples, such as the Akie and Hadza in Tanzania, to coat arrow-tips for hunting.

Propagation: Cuttings, seeds

Properities:
In Adenium obesum the presence of some 30 cardiotoxic glycosides has been demonstrated, which act in a similar way as digitalis from Digitalis. Digitalis acts upon the Na+K+-ATPase enzyme that regulates the concentrations of Na+ and K+ ions in body cells and so also modifies the Ca++ concentration. In low doses it is used to treat congestive heart failure (CHF) and heart rhythm problems (atrial arrhythmias), but in high doses it leads to systolic heart failure and death.
Several of the cardiac glycosides from Adenium obesum have oleandrigenin as aglycone moiety, e.g. hongheloside A (with D-cymarose), hongheloside C (with D-cymarose and D-glucose) and 16-acetylstrospeside (with D-digitalose). Other glycosides include: hongheline (composed of digitoxigenin with D-thevetose), somaline (composed of digitoxigenin with D-cymarose) and digitalinum verum (composed of gitoxigenin with D-digitalose and D-glucose). The roots and stems contain the same glycosides and in similar amounts. Oleandrigenin and some of the glycosides derived from it have cytotoxic effects and are being studied as potential components of anticancer drugs.
The ethanol extract of the roots slows down the growth of Bacillus subtilis, but has not shown activity against Pseudomonas aeruginosa, Staphylococcus aureus or Candida albida. Extracts from the root have shown a cytotoxic effect against several carcinoma cell lines. The aqueous stem bark extract is a potential acaricide as it shows high toxicity on all stadia of development of the ticks Amblyomma spp. and Boophilus spp.

Uses
In a wide area of Africa the root sap or sometimes the wood or stem latex of Adenium obesum is used to prepare arrow poison. The poison is popular for hunting large game as it kills quickly and the hunted animal dies within 2 km from the place where it was shot. The Hadza people of Tanzania use the sap by itself or sometimes in combination with poison from Strophanthus eminii Asch. & Pax, while the Duruma people of Kenya use the stem latex, sometimes in combination with the roots and wood of Acokanthera schimperi (A.DC.) Schweinf. or the latex of Synadenium pereskiifolium (Baill.) Guillaumin. The use of Adenium obesum arrow poison is also reported from Senegal, Nigeria and Cameroon. A decoction of the bark and leaves is widely used as fish poison. This use is reported from Nigeria, Cameroon and East Africa. In Mauritania and Senegal preparations from Adenium obesum are used as ordeal poison and for criminal purposes.

Medicinal Uses:
Adenium obesum is important in traditional medicine. In the Sahel a decoction from the roots, alone or in combination with other plants, is used to treat venereal diseases; a root or bark extract is used as a bath or lotion to treat skin diseases and to kill lice, while latex is applied to decaying teeth and septic wounds. In Somalia a root decoction as nose drops is prescribed for rhinitis. In northern Kenya latex is rubbed on the head against lice and powdered stems are applied to kill skin parasites of camels and cattle. The bark is chewed as an abortifacient.
Adenium obesum is planted fairly frequently for its curious form and attractive flowers. Sometimes it is planted as a live fence. In Tanzania it is planted to mark the position of graves. The wood is sometimes used as fuel.

Classification
The genus Adenium has been held to contain as many as twelve species. These are considered by other authors to be subspecies or varieties. A late-20th-century classification by Plazier recognizes five species.

A partial list of regional species/subspecies/varieties are:

Adenium obesum subsp. boehmianum. Namibia, Angola.
Adenium obesum subsp. obesum. Arabia.
Adenium obesum subsp. oleifolium. South Africa, Botswana.
Adenium obesum subsp. socotranum. Socotra.
Adenium obesum subsp. somalense. Eastern Africa.
Adenium obesum subsp. swazicum. Eastern South Africa.
Adenium obesum subsp. arabicum. Arabia.
Adenium multiflorum. Southern Africa, from Zambia south
Disclaimer : The information presented herein is intended for educational purposes only. Individual results may vary, and before using any supplement, it is always advisable to consult with your own health care provider.

Resources
http://en.wikipedia.org/wiki/Adenium
http://database.prota.org/PROTAhtml/Adenium%20obesum_En.htm
http://www.desert-tropicals.com/Plants/Apocynaceae/Adenium_obesum.html

Enhanced by Zemanta
Categories
News on Health & Science

Scientists Find New Way to Fix a Broken Heart

[amazon_link asins=’1501120123,1520519958,B0733VP18J,157921228X,B00EI0QN2W,160550131X,B079RM5CWJ,B00LFW4G8O,B00HIMN5O6′ template=’ProductCarousel’ store=’finmeacur-20′ marketplace=’US’ link_id=’29ca3987-1143-11e8-9f27-070680d876b0′]

A new way to mend damage to the heart has been found by scientists.

CLICK & SEE THE PICTURES

The boffins have devised a method to coax heart muscle cells into re-entering the cell cycle, allowing the differentiated adult cells to divide and regenerate healthy heart tissue after a heart attack, according to studies in mice and rats by Children’s Hospital Boston reported in the July 24th issue of the journal Cell.

If the same mechanisms identified by the researchers can be shown to work in the human heart, it opens up real possibilities for new and more efficient ways to treat people with heart disease, reports The BBC.

Theoretically, it could be used to treat heart attack patients, those with heart failure and children with congenital heart defects.

The key ingredient is a growth factor known as neuregulin1 (NRG1).

Previously, it was believed that the heart was incapable of repairing itself. During prenatal development, heart muscle cells (cardiomyocytes) proliferate but were thought to lose that ability shortly after birth. But, recent research has indicated that the adult cells do have some ability to replace themselves at a low level.

And, the new study provides evidence that this is true – and that NRG1 can ramp up the process significantly.

The Boston team tested the ability of various molecules to spur cell division in cultured cardiomyocytes, including several factors known to drive proliferation of the cells during prenatal development. NRG1 produced the most significant effect, and it was repeated when the factor was injected into adult mice.

When administered to animals who had suffered a heart attack, it promoted regeneration of heart muscle, and improved the overall function of the organ.

Writing in the journal, they said: “We have identified the major elements of a new approach to promote myocardial regeneration.

“Many efforts and important advances have been made toward the goal of developing stem-cell based strategies to regenerate damaged tissues in the heart as well as in other organs.

“The work presented here suggests that stimulating differentiated cardiomyocytes to proliferate may be a viable alternative.”

Professor Jeremy Pearson, associate medical director of the British Heart Foundation, said: “This fascinating study shows, remarkably, that a significant fraction of adult heart cells in mice can be made to replicate and help to repair damaged hearts.

“If the same mechanisms identified by the researchers can be shown to work in the human heart, it opens up real possibilities for new and more efficient ways to treat people with heart disease.”

Click to see:->

Mending Broken Heart

Can Seaweed Mend a Broken Heart?

Source: The Times Of India

Reblog this post [with Zemanta]
Categories
Health Alert

Fit Enough to Fly

[amazon_link asins=’B01MCZ066G,B00VIQBQQM,B01LYYFONN,B01N30Q7IN,B01KXHGCDI,B012D5KHO8,B01KAAOAR8,B01LCFV8CA,B01LXAJNYD’ template=’ProductCarousel’ store=’finmeacur-20′ marketplace=’US’ link_id=’9cd97710-36d9-11e7-bdfc-650439e98412′]

Families are scattered all over  the globe and they travel to stay in touch. Airplanes are safe, despite the high flying altitude, relatively lower partial pressure of oxygen, variable air circulation, low humidity, sustained periods of noise, vibration and turbulence.
…………….
The rapid changes that occur during a flight (typically during descent) can give rise to ear pain, a blocked feeling, ringing in the ears, giddiness, hearing loss or even rupture of the eardrum. These complications are more likely if the Eustachian tube (connecting the ear and throat) is blocked by allergy, colds, sinusitis or middle ear infections. Chewing gum and frequent swallowing during descent can help ease the discomfort.

Decongestant nose drops will clear a blocked nose. Air travel should be avoided for 10 days if there has been a recent ear surgery or tonsillectomy.

Women often need to travel during pregnancy — as part of their jobs, because of transfers or simply to head home to have the baby. Air travel during pregnancy is safe and poses no special risks. Mid pregnancy, from the 14th to 28th week, is the safest time. In the case of multiple pregnancy (twins), a history of premature delivery, cervical incompetence, bleeding or increased uterine activity (irritable uterus), flying is inadvisable. If you need to be elsewhere for the delivery, it is better to leave before the 36th week or use an alternative mode of transport.

Most airlines refuse to allow pregnant passengers after the 36th week because of the fear that labour may set in during the flight. It is better to carry certified medical documentation about the expected date of delivery.

During pregnancy,

• the seat belt should be fastened under the abdomen, not across it;

• an aisle seat is preferable to facilitate visits to the toilet;

• try to get out of the seat every 30 minutes and walk a short distance;

• if this is not possible, flex and extend the ankles.

Babies should, preferably, not fly till they are at least seven days old.

There is a 10-day ban on air travel (not prohibited but inadvisable) after a stroke, brain surgery, an epileptic seizure, eye surgery or ear, nose or throat procedures.

Even in normal people abdominal gas increases by 25 per cent during air travel. A three to four week gap is advisable after abdominal surgery even if it is a “keyhole” or laparoscopic surgery as gas is introduced into the abdomen during the procedure. This extra gas can expand and cause the sutures to give way.

A person with congestive cardiac failure (when the heart does not function properly) should be stable for at least 10 days prior to travel.

In the case of a heart attack the person should have been stable for three to four weeks.

After pneumonia or chest surgery, a person should wait for three weeks
. Even after this time they should be able to walk unassisted for at least 50 metres without becoming breathless.

Anaemia, with haemoglobin count less than 7.5 grams per decilitre, reduces the oxygen carrying capacity of blood. This can get critical during flights.

People with fractures can travel two days after the cast has been applied. In traditional casts air can be trapped between the cast and the leg. As this air expands during the flight, it can compress the limb and cut off blood supply. If a person needs to fly immediately, the doctor needs to be informed beforehand. A bivalved or split cast, which does not trap air, can be applied.

People with mental illness should be well controlled, on medication and preferably have a companion.

Diseases are spread from one country to another by infected travellers. In the recent swine flu epidemic, the spread of the disease could be plotted by tracking the flights out of Mexico (where the epidemic started).

People with open tuberculosis or measles should also defer travel.
If a person has an infectious disease, travelling should be postponed until recovery. Infected air keeps circulating in a plane and this will result in the disease spreading.

The economy class has little legroom. The edge of the seat can compress the veins at the bent knee.
Together with the forced immobility, blood pools in the legs and the feet swell. This can result in deep vein thrombosis and pulmonary embolism. Sudden unexpected death can occur hours or days after travel.

Generally, try to drink plenty of fluids and balance any alcohol consumed with an equal amount of water. Walk around the airport while waiting. Remember, the most dangerous thing to do is to sit still with your legs crossed.

Source: The Telegraph (Kolkata, India)

Reblog this post [with Zemanta]
css.php