THE DESTINATION

MENINGITIS - when brain suffers

2007-09-23T18:43:00.000+05:30

Introduction
Meningitis is an inflammation of the membranes (meninges) and cerebrospinal fluid surrounding your brain and spinal cord, usually due to the spread of an infection.
In the past, most meningitis cases occurred in children younger than 5 years. But as a result of the protection offered by current childhood vaccines, most meningitis cases now occur in young people between the ages of 15 and 24. Older adults also tend to have a higher incidence of meningitis than do young children.
The cause of most cases of meningitis is a viral infection, but bacterial and fungal infections also can lead to meningitis. The severity of the inflammation and the best treatment depend on the cause of the infection. Bacterial meningitis is generally much more serious than viral meningitis, and timely treatment is necessary.
Left untreated, bacterial meningitis can be fatal. If you suspect that you or someone in your family has signs or symptoms of meningitis, seek medical care right away. There's no way to tell what kind of meningitis you have without seeing your doctor and undergoing testing.

Signs and symptoms
It's easy to mistake the early signs and symptoms of meningitis for the flu. They may develop over a period of one or two days and typically include:
A high fever
Severe headache
Vomiting or nausea with headache
Confusion, or difficulty concentrating — in the very young, this may appear as inability to maintain eye contact
Seizures
Sleepiness or difficulty waking up
Stiff neck
Sensitivity to light
Lack of interest in drinking and eating
Skin rash in some cases, such as in viral or meningococcal meningitis
Earlier signs and symptoms that may suggest a serious infection, although not necessarily meningitis, include leg pain, ice-cold hands and feet, and abnormally pale skin tone.
Signs in newborns

Newborns and young infants may not have the classic signs and symptoms of headache and stiff neck. Instead, they may cry constantly, seem unusually sleepy or irritable, and eat poorly. Sometimes the soft spots on an infant's head may bulge. A very late sign may be a spasm consisting of extreme hyperextension of the body (opisthotonos).
If you or your child has bacterial meningitis, delaying treatment increases the risk of permanent brain damage. In addition, bacterial meningitis can prove fatal in a matter of days. Seek medical care right away if you or anyone in your family has any signs or symptoms.

CAUSES

Meningitis usually results from a viral infection, but the cause also may be a bacterial infection. Less commonly, a fungal infection may cause meningitis. Because bacterial infections are the most damaging, identifying the source of the infection is an important part of developing a treatment plan.
Bacterial meningitis

Acute bacterial meningitis usually occurs when bacteria enter the bloodstream and migrate to the brain and spinal cord. But it can also occur when bacteria invade the meninges directly, as a result of an ear or sinus infection or a skull fracture.
A number of strains of bacteria can cause acute bacterial meningitis. The most common include:
Streptococcus pneumoniae (pneumococcus). This bacterium is the most common cause of bacterial meningitis in infants and young children in the United States. It can also cause pneumonia and ear and sinus infections. When pneumococcal meningitis is associated with an ear infection, it's not always clear which came first — the meningitis or the ear infection — because they usually occur together.
Neisseria meningitidis (meningococcus). This bacterium is another leading cause of bacterial meningitis. Meningococcal meningitis commonly occurs when bacteria from an upper respiratory infection enter your bloodstream. This infection is highly contagious and may cause local epidemics in college dormitories and boarding schools and on military bases.
Haemophilus influenzae (haemophilus). Before the 1990s, Haemophilus influenzae type b (Hib) bacterium was the leading cause of bacterial meningitis. But new Hib vaccines — available as part of the routine childhood immunization schedule in the United States — have greatly reduced the number of cases of this type of meningitis. When it occurs, it tends to follow an upper respiratory infection, ear infection (otitis media) or sinusitis.
Listeria monocytogenes (listeria). These bacteria can be found almost anywhere — in soil, in dust and in foods that have become contaminated. Contaminated foods have included soft cheeses, hot dogs and luncheon meats. Many wild and domestic animals also carry the bacteria. Fortunately, most healthy people exposed to listeria don't become ill, although pregnant women, newborns and older adults tend to be more susceptible. Listeria can cross the placental barrier, and infections in late pregnancy may cause a baby to be stillborn or die shortly after birth.
Viral meningitis

Viral meningitis is usually mild and often clears on its own in 10 days or less. A group of common viruses known as enteroviruses, which cause stomach flu, are responsible for about 90 percent of viral meningitis in the United States.
The most common signs and symptoms of enteroviral infections are rash, sore throat, joint aches and headache. Many older children and adults with enteroviral meningitis describe the "worst headache I've ever had." These viruses tend to circulate in late summer and early fall. Viruses associated with mumps, herpes infection, West Nile virus or other diseases also can cause viral meningitis.
Chronic meningitis

Ongoing (chronic) forms of meningitis occur when slow-growing organisms invade the membranes and fluid surrounding your brain. Although acute meningitis strikes suddenly, chronic meningitis develops over four weeks or more. Nevertheless, the signs and symptoms of chronic meningitis — headaches, fever, vomiting and mental cloudiness — are similar to those of acute meningitis. This type of meningitis is rare.
Fungal meningitis

Fungal meningitis is relatively uncommon. Cryptococcal meningitis is a fungal form of the disease that affects people with immune deficiencies, such as AIDS. It's life-threatening if not treated with an antifungal medication.
Other causes

Meningitis can also result from noninfectious causes, such as drug allergies, some types of cancer and inflammatory diseases such as lupus.

Treatment
Acute bacterial meningitis requires prompt treatment with intravenous antibiotics to ensure recovery and reduce the risk of complications. The antibiotic or combination of antibiotics that your doctor may choose depends on the type of bacteria causing the infection. Often, analyzing a sample of cerebrospinal fluid can help identify the bacteria. If you or your child has bacterial meningitis, your doctor may recommend a broad-spectrum antibiotic until he or she can determine the exact cause of the meningitis.
If you or your child has bacterial meningitis, your doctor may recommend treatments for brain swelling, shock, convulsions or dehydration. Infected sinuses or mastoids — the bones behind the outer ear that connect to the middle ear — may need to be drained. Any fluid that has accumulated between the brain and the membranes that surround it may also need to be drained or surgically removed.
Antibiotics can't cure most viral meningitis, but many cases improve on their own in a week or so without therapy. Treatment of mild cases of viral meningitis is usually with bed rest, plenty of fluids and over-the-counter pain medications to help reduce fever and relieve body aches. If the cause of your meningitis is the herpes virus, your doctor may also recommend an antiviral medication aimed at this virus.

Complications
The complications of meningitis can be severe. The longer you or your child has the disease without treatment, the greater the risk of seizures and of permanent neurological damage, including hearing loss, blindness, loss of speech, learning disabilities, behavior problems and brain damage, even paralysis.
Non-neurological complications may include kidney failure and adrenal gland failure. Your adrenal glands produce a number of important hormones including cortisol, which helps your body deal with stress.
Bacterial infections of your central nervous system progress quickly. Within a matter of days, the disease can lead to shock and death.

BELL'S PALSY - can't accept a deviation

2007-09-22T20:30:00.000+05:30

Introduction
Bell's palsy is a weakness or paralysis of the muscles that control expression on one side of your face. The disorder results from damage to one of a pair of facial nerves that runs beneath each ear to the muscles in your face.
The condition may result in a droopy appearance of your face. This can be a blow to your self-esteem, but most often Bell's palsy isn't serious.
The problem can occur at any age. Bell's palsy occurs more often in pregnant women, in people with diabetes or upper respiratory ailments, such as the flu or a cold, and in people with conditions that compromise their immune systems. Also called facial palsy, Bell's palsy is named for Dr. Charles Bell, a 19th-century surgeon from Scotland who first described the condition.
Bell's palsy clears up on its own within weeks or months for most people. In some cases, doctors prescribe a corticosteroid medication within the first few days, hoping to increase the likelihood of a good recovery.

SIGNS AND SYMPTOMS

Signs and symptoms of Bell's palsy may include:
Sudden onset of paralysis or weakness on one side of your face, making it difficult to smile or close your eye on the affected side
Facial droop and difficulty with facial expressions
Facial stiffness or a feeling that your face is being pulled to one side
Pain behind or in front of your ear on the affected side
Sounds that seem louder on the affected side
Pain, usually in the ear on the affected side
Headache
Loss of taste on the front portion of your tongue
Changes in the amount of tears and saliva your body produces
The severity of Bell's palsy can range from mild weakness to total paralysis on one side of your face. The onset of the problem is fairly abrupt, generally becoming apparent within several hours to a day or two. You may notice symptoms when you awaken. Pain in the vicinity of the ear can precede the palsy by a day or two. Weakness or paralysis usually peaks within 48 hours after onset of signs and symptoms. The faster the signs and symptoms progress, the more serious the weakness or paralysis you'll experience.

Causes
Each facial nerve controls all muscles on one side of your face, except for muscles involved in chewing. The cause of Bell's palsy is still unclear, and its development isn't well understood. But many scientists believe that a viral infection — perhaps most commonly by the herpes simplex virus, the same virus that causes cold sores — can cause the facial nerve to become swollen and injured. Impairment of electrical impulses directed to your facial muscles by the damaged nerve results in the weakness or paralysis of these muscles.

Screening and diagnosis
Your doctor may be able to make a preliminary diagnosis of Bell's palsy by looking at your face and asking you to try to move your facial muscles. Other conditions, such as a stroke, infections and tumors, also may cause facial muscle weakness, mimicking Bell's palsy.
If after a few days there's still doubt about the diagnosis, your doctor may recommend other tests:
Electromyography (EMG). This test can confirm the presence of nerve damage and determine its severity. An EMG can measure the electrical activity of a muscle in response to stimulation and the nature and speed of the conduction of electrical impulses along a nerve.
Brain imaging. This kind of test isn't always necessary, but a test such as magnetic resonance imaging (MRI) or computed tomography (CT) may be needed on occasion to eliminate possible sources of pressure on the facial nerve, such as an infection, tumor or skull fracture.

Complications
Although a mild case of Bell's palsy normally disappears within a month, recovery from a case involving total paralysis varies. If the damage to your facial nerve is unusually severe, the fibers may be irreversibly damaged. Another complication can arise from misdirected regrowth of nerve fibers, which can result in involuntary contraction of certain muscles when you're trying to move others (synkinesis). For example, when you smile, the eye on the affected side may close.

Treatment
Doctors aren't sure that any treatment changes the ultimate outcome of Bell's palsy in most people. Most recover fully with or without treatment.
Courses of treatment may include:
Anti-inflammatory medication. A short course of prescription corticosteroid medication, such as prednisone, may reduce inflammation and swelling in the narrow, bony channel through which the facial nerve travels.
Antiviral medication. Prescription antiviral medications, such as acyclovir (Zovirax) and famciclovir (Famvir), may limit or reduce damage to the nerve from some viral causes.
Massage. Facial massage may help prevent permanent contractures of the paralyzed muscles before recovery takes place.

GLAUCOMA - not everyone escapes

2007-09-21T20:38:00.000+05:30

Introduction
Glaucoma is sometimes called the silent thief because it can slowly steal your sight before you realize anything's wrong. It's a leading cause of vision loss.
The most common form of glaucoma, primary open-angle glaucoma, develops gradually, giving no warning signs. Many people aren't even aware they have an eye problem until their vision is extensively compromised.
Glaucoma is not just one disease, but a group of them. The common feature of these diseases is damage to the optic nerve, usually accompanied by an abnormally high pressure inside your eyeball.
The optic nerve is a bundle of more than a million nerve fibers at the back of your eye. It's like an electric cable made up of thousands of individual wires carrying the images from the inside back wall of your eyeball (retina) to your brain. Blind spots develop in your visual field when the optic nerve deteriorates, usually starting with your peripheral (side) vision. If left untreated, glaucoma may lead to blindness in both eyes.
Fortunately, medical advances have made it easier to diagnose and treat glaucoma. If detected and treated early, glaucoma need not cause even moderate vision loss. But having glaucoma does mean regular monitoring and treatment for the rest of your life.
Signs and symptoms
Glaucoma occurs in several types, and signs and symptoms vary depending on the type of glaucoma you have.
Primary open-angle glaucoma progresses with few or no symptoms until the condition reaches an advanced stage. As increased eye pressure continues to damage your optic nerve, you lose more and more of your peripheral vision. If glaucoma is left untreated, you can develop tunnel vision and eventually lose all sight. Open-angle glaucoma usually affects both eyes, although at first you may have vision loss in just one eye.
Acute angle-closure glaucoma develops suddenly in response to a rapid rise in eye pressure. Permanent vision loss can occur within a day of the attack, so it requires immediate medical attention. An attack often happens in the evening or in a darkened room when the light is dim and your pupils have become relatively dilated. Pain may be severe. Signs and symptoms include:
Blurred vision
Halos around lights
Reddening of the eye
Severe eye pain
Nausea and vomiting
Both open-angle and angle-closure glaucoma can be primary or secondary conditions. They're called primary when the cause is unknown. They're called secondary when the condition can be traced to a known cause, such as an injury or an eye disease. Signs and symptoms of secondary glaucoma vary and depend on what's causing the glaucoma.

CAUSES
Internal pressure in your eye, called intraocular pressure, allows your eye to hold its shape and function properly. Intraocular pressure is like air in a balloon — too much pressure inside the balloon affects its shape and may even cause it to pop. In the case of your eye, too much pressure can damage the optic nerve.
Fluids inside your eye help maintain the intraocular pressure. These fluids are the vitreous, which fills the vitreous cavity at the back of your eye, and the aqueous humor, which fills the anterior chamber at the front of your eye. Aqueous humor is continuously produced and circulated through the anterior chamber before draining out of your eye. This continuous flow of fluid nourishes the lens and the cornea and also removes unwanted debris. A healthy eye produces aqueous humor at the same rate that it drains fluid, thus maintaining a normal pressure.

Risk factors
If the internal pressure in your eye (intraocular pressure) is higher than what's considered normal, you're at increased risk of developing glaucoma, though not everyone with elevated intraocular pressure develops the disease. This makes it difficult to predict who will get glaucoma.
Certain other factors increase your risk. Because chronic forms of glaucoma can destroy vision before any signs or symptoms are apparent, be aware of these factors:
Age. Age is a large risk factor in the development of glaucoma. Everyone older than 60 is at increased risk of the disorder. For blacks however, the increase in risk becomes apparent earlier, after age 40.
Race. Blacks are significantly more likely to get glaucoma than are whites, and they are much more likely to suffer permanent blindness as a result. Mexican-Americans also face an increased risk. Asian-Americans are at higher risk of angle-closure glaucoma, and Japanese-Americans are more prone to low-tension glaucoma. The reasons for these differences aren't clear.
Family history of glaucoma. If you have a family history of glaucoma, you have a much greater risk of developing glaucoma. Glaucoma may have a genetic link, meaning there's a defect in one or more genes that may cause certain individuals to be more susceptible to the disease.
Medical conditions. Diabetes increases your risk of developing glaucoma. A history of high blood pressure or heart disease also can increase your risk, as can hypothyroidism. Routine use of coffee has recently been found to be associated with a slight increase in intraocular pressure.
Physical injuries. Severe trauma, such as being hit in the eye, can result in increased eye pressure. Injury can also dislocate the lens, closing the drainage angle. Other risk factors include retinal detachment, eye tumors, and eye inflammations such as chronic uveitis and iritis. Certain types of eye surgery also may trigger secondary glaucoma.
Nearsightedness. Being nearsighted, which generally means that objects in the distance look fuzzy without glasses or contacts, increases the risk of developing glaucoma.
Prolonged corticosteroid use. Using corticosteroids for prolonged periods of time appears to put you at risk of getting secondary glaucoma.
Eye abnormalities. Structural abnormalities of the eye can lead to secondary glaucoma. For example, pigmentary glaucoma is a form of secondary glaucoma caused by pigment granules being released from the back of the iris. These granules can block the trabecular meshwork.

Screening and diagnosis
If your doctor suspects that you have glaucoma, he or she may perform a series of tests to detect any signs of damage. Tests include:
Tonometry. Tonometry is a simple, painless procedure that measures your intraocular pressure. It is usually the initial screening test for glaucoma.etry
Two common techniques are air-puff tonometry and applanation tonom.
Air-puff tonometry uses a puff of air to measure the amount of force needed to indent your cornea. An applanation tonometer is a sophisticated device that's usually fitted to a slit lamp. Slit lamps use an intense line of light — a slit — providing illumination of the cornea, iris, lens and anterior chamber, and allowing your doctor a good view of these structures.
With tonometry, your doctor numbs your eyes with drops and has you sit behind the slit lamp, where a small flat-tipped cone pushes lightly against your eyeball. The force required to flatten (applanate) a small area of your cornea translates into a measure of your intraocular pressure .
Average normal eye pressures range from 10 to 21 or 22 millimeters of mercury (mm Hg), though most pressures are within 14 to 16 mm Hg. Doctors consider anyone with eye pressure greater than 22 mm Hg to be at risk of developing glaucoma and in need of careful monitoring for early signs of glaucoma.
Tonometry readings vary somewhat depending on a variety of factors including the thickness of your corneas and whether you've had laser surgery on your eyes. For these reasons, newer technologies are being investigated to improve the standard applanation instrument and obtain more accurate intraocular eye pressure measurements.
Test for optic nerve damage. To check the fibers in your optic nerve, your eye doctor uses an instrument called an ophthalmoscope or biomicroscope, which enables him or her to look directly through the pupil to the back of your eye. Your doctor may also use laser light and computers to create a three-dimensional image of your optic nerve. This can reveal slight changes that may indicate the beginnings of glaucoma. Your doctor may also make a detailed drawing of your optic nerves and take photographs of the optic nerves in order to monitor any changes that might occur at future visits.
Visual field test. To check how your visual field has been affected by glaucoma, your doctor uses a perimetry test. One method, known as tangent screen perimetry, requires you to look at a screen with a target in the center. Your eye doctor or a technician manipulates a small object on a wand at different locations in your visual field. You indicate whenever you see the object come into view. By repeating this process over and over again, your entire visual field can be mapped.
Pachymetry. Your eyes are numbed for this test, which uses an ultrasonic-wave instrument to gauge the thickness of each cornea. The thickness of your corneas is an important factor for accurately diagnosing glaucoma. If you have thick corneas, your eye pressure reading may seem high even though you don't have glaucoma. Conversely, people with thin corneas can have low pressure readings, but have glaucoma.
Other tests. To distinguish between open-angle glaucoma and angle-closure glaucoma, your eye doctor may use a technique called gonioscopy (go-ne-OS-kuh-pe), in which a special lens with an angled mirror is placed on your eye to inspect the drainage angle. Another test, tonography, can measure how fast fluid drains through the trabecular meshwork.
To establish a diagnosis of glaucoma, several factors must be present:
Elevated intraocular pressure
Areas of vision loss
Damage to your optic nerve
In glaucoma, the optic disk shows visible signs of damage. The optic disk is the area where all of the nerve fibers come together at the back of your eye before exiting your eyeball. An optic disk that has been affected by glaucoma appears indented, or excavated, as if someone scooped out part of the center of the disk. This condition is known as cupping. The normal contour and color of the disk may also be affected by the loss of nerve fibers.

Treatment
The treatment of glaucoma is aimed at reducing intraocular pressure by improving aqueous outflow, reducing the production of aqueous, or both. Doctors accomplish these treatment goals with eyedrops, systemic medications, laser treatment, surgery, or a combination of treatments.
If your doctor determines that you have elevated intraocular pressure , an excavated optic disk and loss of visual field, you'll likely be treated for glaucoma. If you have only slightly elevated eye pressure, an undamaged optic nerve and no visual field loss, you may not need treatment, but your doctor may advise more frequent examinations to detect any future changes. If you have signs of optic nerve damage and visual field loss, even if your eye pressure is in the normal range, you may need treatment to lower eye pressure further, which may help slow the progression of glaucoma.
Glaucoma can't be cured, and damage caused by the disease can't be reversed. But with treatment, glaucoma can be controlled. Eyedrops, oral medications and surgical procedures can prevent or slow further damage.
Lifelong treatmentHaving glaucoma means you'll need to continue treatment for the rest of your life. Because the disease can progress or change without your being aware of it, your treatment may need to be adjusted over time. Regular checkups and adherence to a treatment plan may seem burdensome, but they're essential to prevent vision loss.
Keeping your eye pressure under control can prevent further damage to the optic nerve and continued loss of your visual field. Your eye doctor may focus on lowering your intraocular pressure to a level that's unlikely to cause further optic nerve damage. This level is often referred to as the target pressure and will probably be a range rather than a single number. Target pressure differs for each person, depending on the extent of the damage and other factors. Your target pressure may change over the course of your lifetime.
Topical eye medications are the most common early treatment for glaucoma. Reducing the pressure in the eyes has been shown to reduce the progression of visual field loss. Standard practice has been to move on to surgery if medications are ineffective or if the glaucoma patient has difficulty in adhering to the medical therapy recommendations. However, surgery is also a relatively safe and effective initial treatment.
EyedropsGlaucoma treatment often starts with medicated eyedrops. Doctors prescribe several types of drops. Be sure to use the drops exactly as prescribed to control your intraocular pressure . Skipping even a few doses can cause damage to the optic nerve to worsen. Some drops need to be applied several times each day, and others must be used just once a day. Inform your doctor of all other medications you're taking, to avoid any undesirable drug interactions.
Because some of the eyedrops are absorbed into your bloodstream, you may experience side effects unrelated to your eyes. To minimize this absorption, close your eyes for one to two minutes after putting the drops in. Press lightly at the corner of your eye near your nose to close the tear duct, and wipe off any unused drops from your eyelid. Your doctor may prescribe more than one type of eyedrop. If you're using more than one, ask your doctor how long to wait between applications.
The types of eyedrops that doctors most commonly prescribe include:
Beta blockers. These reducethe production of aqueous humor. Examples include levobunolol (Betagan), timolol (Betimol, Timoptic), carteolol (Ocupress), betaxolol (Betoptic) and metipranolol (OptiPranolol). Possible side effects include difficulty breathing, slowed pulse, hair loss, lower blood pressure, impotence, fatigue, weakness, depression and memory loss. If you have asthma, bronchitis or emphysema or if you have diabetes and use insulin, medications other than beta blockers may be recommended because beta blockers may worsen breathing problems.
Alpha-adrenergic agents. These reduce the production of aqueous humor. Examples includeapraclonidine (Iopidine) and brimonidine (Alphagan). Possible side effects include fatigue, dizziness, red, itchy or swollen eyes, dry mouth and allergic reactions.
Carbonic anhydrase inhibitors. These medications, which include dorzolamide (Trusopt) and brinzolamide (Azopt), reducethe amount of aqueous humor. Possible side effects include frequent urination and a tingling sensation in the fingers and toes, but these occur more frequently when a carbonic anhydrase inhibitor is taken orally. If you have an allergy or sensitivity to sulfa drugs, don't use these medications unless there's no alternative.
Prostaglandin analogues. These eyedrops increase theoutflow of aqueous humor. These hormone-like substances, which include latanoprost (Xalatan), bimatoprost (Lumigan) and travoprost (Travatan), may be used in conjunction with a drug that reduces production of aqueous humor. There has been a trend away from using these agents as a first line therapy for glaucoma. Possible side effects include mild reddening and stinging of the eyes and darkening of the iris, changes in the pigment of the eyelid skin, and blurred vision from swelling of the retina.
Miotics. Miotics, such as pilocarpine (Isopto Carpine, Pilocar), increase the outflow of aqueous humor. Possible side effects include pain around or inside the eyes, brow ache, blurred or dim vision, nearsightedness, allergic reactions, a stuffy nose, sweating, increased salivation, and occasional digestive problems.
Epinephrine compounds. These also increasethe outflow of aqueous humor. Possible side effects include red eyes, allergic reactions, palpitations, an increase in blood pressure, headache and anxiety.
Oral medicationsIf eyedrops alone don't bring your eye pressure down to the desired level, your doctor may also prescribe an oral medication. Doctors commonly prescribe carbonic anhydrase inhibitors, such as acetazolamide and methazolamide, for glaucoma. Take these pills with meals to reduce side effects. You can help to minimize the potassium loss that these medications can cause by adding bananas and apple juice to your diet.
When you first start taking these oral medications, you may experience a frequent need to urinate and a tingling sensation in your fingers and toes. After several days, these symptoms usually disappear. Other possible side effects of carbonic anhydrase inhibitors include rashes, depression, fatigue, kidney stones, lethargy, stomach upset, a metallic taste in carbonated beverages, impotence and weight loss.
Neuroprotective drugs Lowering the intraocular pressure provides only a partial solution when it comes to preserving vision in people with glaucoma. Several clinical trials are under way to learn if certain drugs may help protect the optic nerve from damage associated with glaucoma. Some are investigating the potential neuroprotective effects of brimonidine (Alphagan), a topical eye medication that may already be prescribed for glaucoma. Another is investigating the potential neuroprotective effect of memantine, an oral medication generally used in the treatment of Alzheimer's disease.

Surgery
You may need surgery to treat glaucoma if you can't tolerate medications or if they're ineffective. Doctors use several types of surgery to treat glaucoma:
Laser surgery. In the last couple of decades, a procedure called trabeculoplasty (truh-BEK-u-lo-plas-te) has been used increasingly in the treatment of open-angle glaucoma. The doctor uses a high-energy laser beam to shrink part of the trabecular meshwork, which causes other parts of the meshwork to stretch and open up. This helps aqueous humor drain more easily from the eye.
This type of laser surgery is an office procedure that takes 10 to 20 minutes. You'll be given an anesthetic eyedrop, seated at a slit lamp and fitted with a special lens on your eye. The doctor aims the laser through the lens at the trabecular meshwork and applies burns to it. You will see bright flashes of light.
Usually, you can immediately resume normal activities without discomfort. The doctor will usually check your eye pressure one to two hours after the procedure and several times in the following weeks. It may take a few weeks before the full effect of the surgery becomes apparent.
In almost all cases, laser surgery for glaucoma initially lowers intraocular pressure. After time, however, intraocular pressure may begin to increase.
Conventional surgery. If eyedrops and laser surgery aren't effective in controlling your eye pressure, you may need an operation called a filtering procedure, usually in the form of a trabeculectomy (truh-bek-u-LEK-tuh-me). This procedure is done in a hospital or an outpatient surgery center.
You'll receive medication to help you relax and eyedrops and usually an injection of anesthetic to numb your eye. Using delicate instruments under an operating microscope, your surgeon creates an opening in the sclera — the white of your eye — and removes a small piece of the trabecular meshwork.
The aqueous humor can now freely leave the eye through this hole. As a result your eye pressure will be lowered. The hole is covered by the conjunctiva, so there's not an open hole in your eye. This procedure works best if you haven't had any previous eye surgery.
Your doctor will check your eye during several follow-up visits. You'll need to use antibiotic and anti-inflammatory eyedrops for some time after the operation to fight infection and scarring of the newly created drainage opening. Scarring is a particular problem for young adults, blacks and people who have had cataract surgery.
Although glaucoma surgery may preserve current vision, it can't restore already lost vision. Sometimes a single surgical procedure may not lower eye pressure enough, in which case you'll need to continue using glaucoma drops or have another trabeculectomy operation.
Drainage implants. Another type of operation, called drainage implant surgery, may be an option for people with secondary glaucoma or for children with glaucoma. Like the trabeculectomy, drainage implant surgery is performed at a hospital or an outpatient clinic. You'll receive medication to help you relax and eyedrops and an anesthetic to numb your eye. Then the doctor inserts a small silicone tube in your eye to help drain aqueous humor.
After the surgery you'll wear an eye patch for 24 hours and use eyedrops for several weeks to fight infection and scarring. Your doctor will check your eyes several times in the weeks that follow.
Possible complications from glaucoma surgery may include infection, bleeding, eye pressure that remains too high or too low, and, potentially, loss of vision. Having eye surgery may also speed up the development of cataracts. Most of these complications can be effectively treated.
Treating acute angle-closure glaucoma Acute angle-closure glaucoma is a medical emergency. When you come in with this condition, doctors may administer several medications to reduce eye pressure as quickly as possible. You'll also likely have a laser procedure called iridotomy (ir-ih-DOT-uh-me).
In this procedure, a laser beam creates a small hole in your iris to allow aqueous humor to flow more freely into the anterior chamber where it then has normal access to the trabecular meshwork. Once aqueous humor can reach the trabecular meshwork again, the fluid can drain as it normally does. Many doctors recommend an iridotomy on the other eye at a later date because of the high risk that it too will have an attack within the next few year.

Prevention
Until recently, there was no proven way to prevent glaucoma. But a large multicenter trial, supported by the National Eye Institute, found that when glaucoma eyedrops were given daily to people with elevated eye pressure (above 24 mm Hg), they reduced eye pressure an average of 22 percent. More important, the researchers discovered that daily use of eyedrops can reduce the risk of developing glaucoma by nearly half in blacks with elevated eye pressure.
Another study found that cholesterol-lowering medications reduced the risk of open-angle glaucoma, especially for people who already have cardiovascular disease. Although this may be an added benefit for those already taking these medications to reduce their cholesterol levels, more studies need to be done to confirm the reduction in risk of glaucoma.
Frequent monitoringRegular checkups can help detect the disease in its early stages before irreversible damage has occurred. As a general rule, have eye exams every two to four years if you're between the ages of 40 and 65, and every one to two years if you're older than 65.
Your doctor will likely recommend more frequent monitoring if you're at increased risk of developing glaucoma. For example, a family history of glaucoma puts you at increased risk of developing glaucoma and is a reason for more frequent monitoring. You may also need even more frequent checkups if you have received a diagnosis of abnormally high intraocular pressure or have a history of serious eye injury.

USE OF ATYPICAL ANTIDEPRESSANTS IN ELDERLY PATIENTS

2007-09-20T17:24:00.000+05:30

INTRODUCTION ----------------------------------------------------------------------------Late-life major depressive disorder (MDD) is a common disorder that is associated with severe symptoms and substantial functional impairment. With an estimated prevalence of 3% in people aged 60 years or more, MDD has growing health implications for the aging population. In addition, MDD is often associated with physical disability in this age group as well as a high mortality rate. Conditions leading to chronic pain, the presence of comorbid medical illnesses, social isolation, and dysphoria secondary to life-cycle issues predispose the elderly population to the development of depression. These factors also point elderly individuals with depression in the direction of more severe symptoms and a relatively poor outcome.
While it is a commonly known psychiatric disorder, depression in the geriatric population is under-recognized and under-treated, leading to unnecessary impaired social and occupational functioning.1 Studies suggest that approximately 25% of patients aged 65 years or more who have a chronic medical illness also experience symptoms of depression. Evidence supports the increased prevalence of depression in several specific chronic medical illnesses, including vascular disease, diabetes mellitus, and arthritis; the relative risk for depression is 2-3 times higher in these patients than in individuals without these comorbidities.1 Depression in the geriatric population has also been reported to be more somatic and less ideational than depression in younger adults. Elderly people who suffer from comorbid depression and medical illness have an increased morbidity and mortality.

1 Authors have also noted a brittle response to antidepressant therapy and an increased risk for chronic depression in the elderly population.

2 Safe, effective, well-tolerated antidepressants are needed for elderly patients with MDD, especially for those who are also struggling with chronic medical illness

TREATMENT OPTIONS FOR MDD IN THE ELDERLY

The evidence supports the use of selective serotonin reuptake inhibitors (SSRIs) as first-line therapy for MDD in all age groups. However, in view of their adverse effect profile and efficacy, atypical antidepressants may also be considered as a primary treatment option.3 The relatively high comorbid prevalence of conditions that lead to chronic pain and depression in the elderly population is of significance, given that a direct relationship between the intensity of pain and the degree of depression has also been established. In this subset of geriatric depression, clinicians should consider the use of serotonin-norepinephrine reuptake inhibitors (SNRIs) such as duloxetine or venlafaxine in view of the combined effect of this class of medication in treating both depression and the chronic pain condition.

1 .Studies also suggest that antidepressant drugs that combine the serotonergic and noradrenergic mechanisms of action are of comparable efficacy to SSRIs and may even be modestly more effective in the treatment of MDD. Studies also suggest that treatment with venlafaxine may be effective in geriatric patients with treatment-resistant MDD and is better tolerated than prescribing additional medication to augment antidepressant treatment.

PHARMACOLOGY AND PHARMACOKINETICS OF ATYPICAL ANTIDEPRESSANT SSNRIs

Block the reuptake of both serotonin (5-HT) and norepinephrine with differing selectivity. They have been shown to be superior to placebo and have comparable efficacy to the tricyclic antidepressants (TCAs). SNRIs include venlafaxine and duloxetine and have an adverse effect profile similar to that of the SSRIs.5 A difference, however, between this class of antidepressants and other classes is the ability of SNRIs to effectively treat chronic pain irrespective of whether the pain is related to depression or unrelated.6 In addition to treating depression, duloxetine may also offer a new treatment for patients with neuropathic pain and stress urinary incontinence.7 Adverse effects specific to individual drugs have been documented; venlafaxine has been associated with hypertension and duloxetine has been associated with hepatotoxicity.
The dopamine-norepinephrine reuptake inhibitor (DNRI) bupropion primarily blocks the reuptake of dopamine and norepinephrine with no direct action on the serotonin system.8 Bupropion has been shown to have efficacy comparable to both TCAs and SSRIs in the treatment of MDD.5 Bupropion has a lower risk of sexual dysfunction and weight gain than some other antidepressants and is an effective alternative or adjunctive treatment for patients whose symptoms do not respond to SSRIs.8 Compared to SSRIs, treatment with bupropion has the disadvantage of an increased adverse effect profile that includes headaches, tremors, and seizures. The risk of seizures decreases at doses less than 450 mg and with divided dosing.5
The norepinephrine-serotonin modulator mirtazapine enhances the release of norepinephrine by blocking α2-adrenergic autoreceptors as well as serotonin 5-HT2A and 5-HT3 receptors and histamine H1 receptors. Its efficacy is similar to that of TCAs and SSRIs, and it is less likely to cause sexual adverse effects. Mirtazapine has been associated with weight gain and sedation, which can be helpful for patients who are also experiencing decreased appetite and insomnia.9
Serotonin modulators, which include nefazodone and trazodone, block the 5-HT2A serotonin receptor and serotonin reuptake and have an antidepressant efficacy similar to that of SSRIs. Nefazodone and trazodone and are less commonly used to treat depression because of their adverse-effect profiles of hepatoxicity and sedation, respectively. Trazodone is mainly used in clinical practice for its sedative properties separate from the treatment of depression.

SPECIAL CONSIDERATIONS WHEN PRESCRIBING ATYPICAL ANTIDEPRESSANTS TO ELDERLY PATIENTS

The presence of high levels of pain in elderly patients may diminish the degree of response for the comorbid symptoms of depression for any given antidepressant therapy. The detection, diagnosis, and management of chronic pain should routinely include the identification and treatment of coexisting medical conditions that may contribute to or complicate late-life depression. Both the depression and the comorbid medical condition that is contributing to the depression should be treated from the outset.3
When prescribing an antidepressant to an elderly patient, the initial dose of the agent must be determined by individual symptom response, known adverse effect profile, drug-drug interactions, and any comorbid medical and psychiatric conditions. The initial dose selected may be smaller than that prescribed to younger patients because of age-related physiological changes such as impaired hepatic and renal elimination that can result not only in higher serum concentrations of the drug for a given dose but also in a higher likelihood of adverse effects. As a general rule of thumb, clinicians should “start low and go slow” when prescribing antidepressants to elderly patients.10
While venlafaxine may be effective and be associated with fewer drug-drug interactions and a generally favorable adverse effect profile, it is associated with some undesirable cardiovascular effects, such as hypertension, orthostatic hypertension, and new-onset tachycardia or palpitations. Systematic monitoring of cardiovascular parameters is strongly recommended in elderly patients, especially those who are taking more than 150 mg of venlafaxine per day.11
Mirtazapine, like SSRIs, has been reported to uncommonly cause hyponatremia. While this adverse effect is uncommon, it should be considered in any elderly patient with altered mental status who has recently started to take mirtazapine.
The issue of drug-drug interactions is of particular relevance for geriatric patients because of the increased likelihood of polypharmacy for comorbid illnesses. Polypharmacy may lead not only to notable adverse effects as a result of the interaction of medications but also to an increased risk of known adverse effects from the prescribed antidepressant. The antidepressants with the least potential for altering drug metabolism are some of the SSRIs, such as citalopram, and the selected atypical antidepressants, such as venlafaxine, duloxetine, and mirtazapine.

Parkinsonism - can u remember

2007-09-19T19:40:00.000+05:30

What is parkinsonism?

Parkinsonism refers to any condition that causes a combination of the movement abnormalities seen in Parkinson's disease — such as tremors, slow movement, impaired speech or muscle stiffness — resulting from the loss of dopamine-containing nerve cells (neurons). The most common cause of parkinsonism is Parkinson's disease. But not everyone who has parkinsonism has Parkinson's disease. Other causes of parkinsonism include:
Stroke
Encephalitis, inflammation of the brain usually caused by infection
Meningitis, inflammation of the membranes covering the brain and spinal cord
Progressive supranuclear palsy, a rare degenerative brain disorder
Multiple systems atrophy, a degenerative disorder that destroys nerve tissue
Corticobasal degeneration, a rare neurological disease
Certain medications, such as some antipsychotics and metoclopramide
Head trauma, isolated or repeated, such as injuries sustained in boxing

signs and symptoms

The earliest symptom of Parkinson's disease can be as subtle as an arm that doesn't swing when you walk, a mild tremor in the fingers of one hand or soft, mumbling speech that's difficult to understand. You may lack energy, feel depressed or have trouble sleeping. Or you may notice that it takes you longer to shower, shave, eat or do other routine tasks.
Other signs and symptoms of Parkinson's disease may include:

Tremor. This often starts with a slight shaking in your hand or even one finger. Sometimes hand tremor causes a back-and-forth rubbing of your thumb and forefinger known as pill-rolling. Tremor may also develop in your legs. These signs may occur on one or both sides of your body and may be more noticeable when you're under stress. Although tremor can be very distressing, it's usually not disabling and often disappears when you're sleeping. Many people with Parkinson's disease do not experience substantial tremor.
Slowed motion (bradykinesia). Over time, Parkinson's disease may cause a slow, shuffling walk with an unsteady gait and stooped posture. And leg muscles may freeze up, making it hard to resume normal movement. This is especially distressing because it can make performing the simplest tasks difficult and time-consuming.
Rigid muscles. Muscle stiffness (rigidity) often occurs in your limbs and neck. Sometimes the stiffness can be so severe that it limits the size of your movements and causes pain.
Impaired balance. Your posture may become unstable as a result of Parkinson's disease. Often this problem remains minor for many years.
Loss of automatic movements. Blinking, smiling and swinging your arms when you walk are all unconscious acts that are a normal part of being human. In Parkinson's disease, these acts tend to be diminished and even lost. Some people may develop a fixed staring expression and unblinking eyes. Others may no longer gesture or seem animated when they speak.
Impaired speech. Many people with Parkinson's disease have some trouble speaking, and their voices often become monotonous and very soft. This may be a special problem for older adults because the soft voice of a person with Parkinson's disease may not be audible to a spouse with poor hearing.
Difficulty swallowing. This may develop in the later stages of the disease, but except in rare cases, most people who have trouble swallowing can continue to eat on their own.
Dementia. A small percentage of people with Parkinson's develop this mental disorder — which affects the ability to think, reason and remember — late in the course of the disease. Although it's often associated with Alzheimer's disease, dementia can also occur with other conditions. In Parkinson's, the onset of dementia is often marked by slowed thought processes and problems with concentration.

Treatment

For many people with Parkinson's, the initial response to treatment can be dramatic. Over time, however, the benefits of drugs frequently diminish or become less consistent, although symptoms can usually still be fairly well controlled. In addition to medications, your doctor may also recommend that you try lifestyle changes, such as physical therapy, a healthy diet and exercise.
Physical therapy, especially, can be extremely helpful for people with Parkinson's disease — both in the early stages and later, as the disease progresses. It can help improve mobility, range of motion and muscle tone. Although specific exercises can't stop the progress of the disease, improving muscle strength can help you feel more confident and capable. A physical therapist can also work with you to improve your gait and balance. For many people, working with a speech pathologist can help improve problems with speaking and swallowing.
When lifestyle changes are no longer enough, your doctor will likely recommend certain medications, either alone or in combination.
MedicationsMedications can help manage problems with walking, movement and tremor by increasing the brain's supply of dopamine. Your medication needs may change over time, and the drug dosage and timing may require adjustment. For these reasons, you and your doctor will work together to design a program that best suits your needs, especially as the disease progresses. The medications used to treat Parkinson's disease include:

MEDICINE

Levodopa and carbidopa.

Dopamine agonists : This class of drugs includes bromocriptine (Parlodel), apomorphine (Apokyn), pramipexole (Mirapex) and ropinirole (Requip).

Selegiline (Eldepryl).

Catechol-O-methyltransferase (COMT) inhibitors.

Anticholinergics.

Amantadine

SURGERY

SurgeryDoctors once commonly used surgical procedures to treat Parkinson's disease. But with the advent of levodopa and other drug therapies, surgical approaches have been re-evaluated. The following procedures may be an option when symptoms can't be controlled with medications:

Thalamotomy

Pallidotomy.

Complications
As many as half the people with Parkinson's disease develop depression. In some cases, depression may occur months or even years before Parkinson's disease is diagnosed. Although physical limitations resulting from Parkinson's disease can be frustrating and stressful, depression in someone with Parkinson's isn't usually a reaction to physical disability. Instead, it more likely arises from underlying brain changes associated with the disease itself.
In addition, some people with Parkinson's disease eventually develop dementia, a condition that can include memory loss, impaired judgment and personality changes.
Medications for Parkinson's disease also may cause a number of complications, including involuntary twitching or jerking movements of the arms or legs (dyskinesia), hallucinations, sleepiness, and a drop in blood pressure when standing up (orthostatic hypotension).
Other complications of Parkinson's disease may include:
Difficulty chewing and swallowing. In the later stages of the disease, the muscles you use to swallow may be affected, making eating more difficult.
Urinary problems. Parkinson's disease may cause either urinary incontinence or urine retention. Certain medications used to treat the disease, especially anticholinergic drugs, also can make it difficult to urinate.
Constipation. Many people with Parkinson's disease develop constipation because the digestive tract works more slowly. Constipation may also be a side effect of medications used to treat the disease.
Sleep problems. People with Parkinson's disease often have trouble falling asleep and may wake up frequently throughout the night. They may also experience restless sleep and even act out their dreams (rapid eye movement sleep behavior disorder).
Sexual dysfunction. Some people with Parkinson's disease may notice a decrease in sexual desire (libido). This may stem from a combination of psychological and physical factors, or it may be the result of physical factors alone.

MYOCARDIAL INFARCTION - you can't let your heart stop beating , can you ?

2007-09-18T19:09:00.000+05:30

What is Ischemic Heart Disease?

Ischemic heart disease is caused by an imbalance between the myocardial blood flow and the metabolic demand of the myocardium. Reduction in coronary blood flow is related to progressive atherosclerosis with increasing occlusion of coronary arteries. Blood flow can be further decreased by superimposed events such as vasospasm, thrombosis, or circulatory changes leading to hypoperfusion.
Coronary artery perfusion depends upon the pressure differential between the ostia (aortic diastolic pressure) and coronary sinus (right atrial pressure). Coronary blood flow is reduced during systole because of Venturi effects at the coronary orifices and compression of intramuscular arteries during ventricular contraction.

Factors reducing coronary blood flow include:

Decreased aortic diastolic pressure
Increased intraventricular pressure and myocardial contraction
Coronary artery stenosis, which can be further subdivided into the following etiologies:
Fixed coronary stenosis
Acute plaque change (rupture, hemorrhage)
Coronary artery thrombosis
Vasoconstriction
Aortic valve stenosis and regurgitation
Increased right atrial pressure
40 micron collateral vessels are present in all hearts with pressure gradients permitting flow, despite occlusion of major vessels. In general, the cross-sectional area of the coronary artery lumen must be reduced by more than 75% to significantly affect perfusion. Coronary atherosclerosis is diffuse (involving more than one major arterial branch) but is often segmental, and typically involves the proximal 2 cm of arteries (epicardial).
"Thrombolytic therapy" with agents such as streptokinase or tissue plasminogen activator (TPA) is often used to try and lyse a recently formed thrombus. Such therapy with lysis of the thrombus can re-establish blood flow in a majority of cases. This helps to prevent significant myocardial injury, if early (less than an hour or so) in the course of events, and can at least help to reduce further damage.

Patterns of Ischemic Heart Disease (IHD)

Angina pectoris - a symptom complex of IHD characterized by paroxysmal attacks of chest pain, usually substernal or precordial, caused by myocardial ischemia that falls short of inducing infarction. There are several patterns:
Stable angina (typical) - paroxysms of pain related to exertion and relieved by rest or vasodilators.subendocardial ischemia with ST-segment depression
Variant or Prinzmetal's angina - angina that classically occurs at rest and is caused by reversible spasm in normal to severely atherosclerotic coronary arteries. ST-segment elevation or depression maybe seen during attacks.
Unstable angina - prolonged pain, pain at rest in a person with stable angina, or worsening of pain in stable angina. ST-segment depression (usually) and ST-segment elevation.
Sudden cardiac death - Unexpected death from cardiac causes usually within one hour after a cardiac event or without the onset of symptoms. Strikes 300,000 - 400,000 persons annually. Usually high-grade stenosis with acute coronary changes.

Myocardial Infarction (MI)

The pathogenesis can include:

Occlusive intracoronary thrombus - a thrombus overlying an ulcerated or fissured stenotic plaque causes 90% of transmural acute myocardial infarctions.
Vasospasm - with or without coronary atherosclerosis and possible association with platelet aggregation.
Emboli - from left sided mural thrombosis, vegetative endocarditis, or paradoxic emboli from the right side of heart through a patent foramen ovale.

The gross morphologic appearance of a myocardial infarction can vary. Patterns include:
Transmural infarct - involving the entire thickness of the left ventricular wall from endocardium to epicardium, usually the anterior free wall and posterior free wall and septum with extension into the RV wall in 15-30%. Isolated infarcts of RV and right atrium are extremely rare.
Subendocardial infarct - multifocal areas of necrosis confined to the inner 1/3-1/2 of the left ventricular wall. These do not show the same evolution of changes seen in a transmural MI.

. Complications can include:
Arrhythmias and conduction defects, with possible "sudden death"
Extension of infarction, or re-infarction
Congestive heart failure (pulmonary edema)
Cardiogenic shock
Pericarditis
Mural thrombosis, with possible embolization
Myocardial wall rupture, with possible tamponade
Papillary muscle rupture, with possible valvular insufficiency
Ventricular aneurysm formation
.
Laboratory Diagnosis of Myocardial Infarction
A number of laboratory tests are available. None is completely sensitive and specific for myocardial infarction, particularly in the hours following onset of symptoms. Timing is important, as are correlation with patient symptoms, electrocardiograms, and angiographic studies.

The following tests are available as markers for acute myocardial infarction:
Creatine Kinase - Total:
The total CK is a simple and inexpensive test that is readily available using many laboratory instruments. However, an elevation in total CK is not specific for myocardial injury, because most CK is located in skeletal muscle, and elevations are possible from a variety of non-cardiac conditions.
Creatine Kinase - MB Fraction:
Creatine kinase can be further subdivided into three isoenzymes: MM, MB, and BB. The MM fraction is present in both cardiac and skeletal muscle, but the MB fraction is much more specific for cardiac muscle: about 15 to 40% of CK in cardiac muscle is MB, while less than 2% in skeletal muscle is MB. The BB fraction (found in brain, bowel, and bladder) is not routinely measured.
Thus, CK-MB is a very good marker for acute myocardial injury, because of its excellent specificity, and it rises in serum within 2 to 8 hours of onset of acute myocardial infarction. Serial measurements every 2 to 4 hours for a period of 9 to 12 hours after the patient is first seen will provide a pattern to determine whether the CK-MB is rising, indicative of myocardial injury. The CK-MB is also useful for diagnosis of reinfarction or extensive of an MI because it begins to fall after a day, dissipating in 1 to 3 days, so subsequent elevations are indicative of another event.
A "cardiac index" can provide a useful indicator for early MI. This is calculated as a ratio of total CK to CK-MB, and is a sensitive indicator of myocardial injury when the CK-MB is elevated.
CK-MB Isoforms:
The CK-MB fraction exists in two isoforms called 1 and 2 identified by electrophoretic methodology. The ratio of isoform 2 to 1 can provide information about myocardial injury.
An isoform ratio of 1.5 or greater is an excellent indicator for early acute myocardial infarction. CK-MB isoform 2 demonstrates elevation even before CK-MB by laboratory testing. However, the disadvantage of this method is that it is skilled labor intensive because electrophoresis is required, and large numbers of samples cannot be run simultaneously nor continuously. False positive results with congestive heart failure and other conditions can occur.
Troponins:
Troponin I and T are structural components of cardiac muscle. They are released into the bloodstream with myocardial injury. They are highly specific for myocardial injury--more so than CK-MB--and help to exclude elevations of CK with skeletal muscle trauma. Troponins will begin to increase following MI within 3 to 12 hours, about the same time frame as CK-MB. However, the rate of rise for early infarction may not be as dramatic as for CK-MB.
Troponins will remain elevated longer than CK--up to 5 to 9 days for troponin I and up to 2 weeks for troponin T. This makes troponins a superior marker for diagnosing myocardial infarction in the recent past--better than lactate dehydrogenase (LDH). However, this continued elevation has the disadvantage of making it more difficult to diagnose reinfarction or extension of infarction in a patient who has already suffered an initial MI. Troponin T lacks some specificity because elevations can appear with skeletal myopathies and with renal failure.
Myoglobin:
Myoglobin is a protein found in skeletal and cardiac muscle which binds oxygen. It is a very sensitive indicator of muscle injury. The rise in myoglobin can help to determine the size of an infarction. A negative myoglobin can help to rule out myocardial infarction.. It is elevated even before CK-MB. However, it is not specific for cardiac muscle, and can be elevated with any form of injury to skeletal muscle.
Lactate dehydrogenase:
The LDH has been supplanted by other tests. It begins to rise in 12 to 24 hours following MI, and peaks in 2 to 3 days, gradually dissipating in 5 to 14 days. Measurement of LDH isoenzymes is necessary for greater specificity for cardiac injury. There are 5 isoenzymes (1 through 5). Ordinarily, isoenzyme 2 is greater than 1, but with myocardial injury, this pattern is "flipped" and 1 is higher than 2. LDH-5 from liver may be increased with centrilobular necrosis from passive congestion with congestive heart failure following ischemic myocardial injury.

TREATMENT

Although symptoms of an acute MI can vary, the typical patient will complain of discomfort in the region of the chest. Other symptoms may include shortness of breath; sweating; lightheadedness and dizziness; pain in other areas of the upper body such as the lower jaw, shoulders, or arms; or gastrointestinal symptoms such as nausea, vomiting, or belching. Some patients having an MI will experience few, if any, symptoms.
INITIAL TREATMENT — Patients who come to an emergency department with symptoms suggesting possible MI all receive the same initial treatment, designed to evaluate the problem and provide initial therapy in the event that an MI is occurring.
The patient is given oxygen through a nasal cannula (a flexible plastic tube that rests beneath the nose) or by a face mask, and an electrocardiogram (ECG) is taken as quickly as possible. The ECG gives a picture of the flow of electrical activity that causes the heart to beat. Damaged areas usually show an abnormal pattern. The ECG may be repeated several times in the first few minutes to monitor for changes that may be occurring. Blood is drawn and sent to the laboratory for routine tests as well as specific tests that look for substances in the blood that are released by damaged heart tissue (cardiac enzymes or proteins).
An intravenous line (IV) is started so that medicines can be given directly into the veins. Nitroglycerin is given either through the IV or under the tongue in an attempt to relieve the chest pain. Morphine may also be given to help relieve the chest pain and to help ease the patient's anxiety. The patient is given aspirin to chew and swallow to help halt the formation of further blood clots. During this time, the patient is carefully questioned about the onset of symptoms, past medical history, and the presence of risk factors that are known to lead to CHD and MI.
In this early stage, the physician is particularly interested in the ECG patterns that emerge. If the patient's history is suggestive of an MI, the characteristics of the ECG will be an important determinant of the next steps in the treatment process; the ECG often yields important information about the location and severity of an MI

Intensive medical therapy — The patient's condition is stabilized with intravenous drugs. After several days, the drugs are stopped. If the patient's symptoms do not return, exercise testing is performed. In this test, the patient exercises on a treadmill or bicycle, and the heart's response is examined using a continuous ECG recording and, often, other scanning techniques using a radioactive tracer that demonstrates blood flow to various parts of the heart. The exercise test can indicate whether narrowing or occlusion of one or more coronary arteries is present.

TREATMENT OF THE COMPLICATIONS OF MI —

Some of the most common complications of MI and a brief description of the treatment options in each case are presented here.
Ongoing ischemia — Early treatments may fail to halt the ischemic process and larger areas of the heart may become damaged. In patients with non-ST elevation MI who are undergoing intensive medical therapy (as opposed to early catheterization), ongoing ischemia would be an indication for a change in approach to immediate catheterization followed by PCI or surgery. In a patient with any type of MI, if catheterization with PCI or surgery is not possible (because it is not available or the patient cannot tolerate the procedure), additional medicine can be used to try to control the ischemia.
Abnormal heart rhythms — The heart has an electrical system, found within the muscle of the heart, that is responsible for stimulating the heart to beat. The damaged heart muscle can cause disturbances in the way the electrical impulses travel within the heart muscle. An erratic heart beat and/or abnormal heart rhythms (arrhythmia) can result. Some of these abnormal rhythms can be dangerous, and can lead to poor heart function. Abnormal rhythms can also result in sudden cardiac death (a cardiac arrest). Drugs can be used to control many types of heart rhythm disturbances. In other cases, a pacemaker is used. In still others, an electrical current is applied to the heart (cardioversion or defibrillation) in an attempt to correct the problem.

Left ventricular aneurysm — This refers to an area of the left ventricle that has become thin and scarred, often bulging out and moving in an ineffective way during contraction. A left ventricular aneurysm can lead to a poorly functioning left ventricle, described above. If the aneurysm is severe, surgery can be done in an attempt to remove the aneurysm and repair the area. In less severe cases, medications that improve ventricular function may be effective.

OTHERS

CARDIAC REHABILITATION — Patients who participate in cardiac rehabilitation following MI receive additional tools they need to stay as healthy as possible. Components of a comprehensive rehabilitation program include:
An exercise prescription — A supervised exercise program specifically for cardiac patients helps them learn to exercise safely in a way that will promote heart health.
Risk factor modification — Patients are given information and advice about controlling factors that can increase the risk of worsening CHD. Risk factor modification includes improving blood cholesterol levels through diet, medication, and exercise; quitting smoking; and treating high blood pressure and elevated blood sugar (diabetes).
Treating the emotional effects of MI and learning to handle stress — A variety of emotions occur in someone who has had an MI. Normal reactions include depression, anxiety, and denial. A cardiac rehabilitation program can help patients learn to deal with these and other emotions in a way that will help promote health and decrease the risk of further cardiac problems.

COPD - The more you smoke, the more you croak

2007-09-17T18:41:00.000+05:30

Chronic obstructive pulmonary disease (COPD) is a lung disease in which the lungs are damaged, making it hard to breathe. In COPD, the airways—the tubes that carry air in and out of your lungs—are partly obstructed, making it difficult to get air in and out.
Cigarette smoking is the most common cause of COPD. Most people with COPD are smokers or former smokers. Breathing in other kinds of lung irritants, like pollution, dust, or chemicals, over a long period of time may also cause or contribute to COPD.
The airways branch out like an upside-down tree, and at the end of each branch are many small, balloon-like air sacs called alveoli (al-VEE-uhl-EYE). In healthy people, each airway is clear and open. The air sacs are small and dainty, and both the airways and air sacs are elastic and springy. When you breathe in, each air sac fills up with air like a small balloon; when you breathe out, the balloon deflates and the air goes out. (See the How the Lungs Work section for details.) In COPD, the airways and air sacs lose their shape and become floppy. Less air gets in and less air goes out because:
The airways and air sacs lose their elasticity (like an old rubber band).
The walls between many of the air sacs are destroyed.
The walls of the airways become thick and inflamed (swollen).
Cells in the airways make more mucus (sputum) than usual, which tends to clog the airways.

The illustration show the respiratory system and cross-sections of healthy alveoli and alveoli with COPD.
COPD develops slowly, and it may be many years before you notice symptoms like feeling short of breath. Most of the time, COPD is diagnosed in middle-aged or older people.
COPD is a major cause of death and illness, and it is the fourth leading cause of death in the United States and throughout the world.
There is no cure for COPD. The damage to your airways and lungs cannot be reversed, but there are things you can do to feel better and slow the damage.
COPD is not contagious—you cannot catch it from someone else.

Conjunctivitis - eyes are not spared

2007-09-16T21:33:00.000+05:30

Conjunctivitis :

(commonly called "pinkeye" or bloodshot eyes in the USA and "Madras Eye" in India) is an inflammation of the conjunctiva (the outermost layer of the eye and the inner surface of the eyelids), most commonly due to an allergic reaction or an infection (usually bacterial or viral).
Blepharoconjunctivitis is the combination of conjunctivitis with blepharitis (inflammation of the eyelids).
Keratoconjunctivitis is the combination of conjunctivitis and keratitis (corneal inflammation).
Episcleritis is an inflammatory condition that produces a similar appearance to conjunctivitis, but without discharge or tearing.

Diagnosis :-

Symptoms :

Eyes with conjunctivitis.
Redness, irritation and watering of the eyes are symptoms common to all forms of conjunctivitis. Itch and the closing of the throat is variable.
Acute allergic conjunctivitis is typically itchy. Sometimes distressingly so, and the patient often complains of some lid swelling. Chronic allergy often causes just itch or irritation, and often much frustration because the absence of redness or discharge can lead to accusations of hypochondria.
Viral conjunctivitis is often associated with an infection of the upper respiratory tract, a common cold, or a sore throat. Its symptoms include watery discharge and variable itch. The infection usually begins with one eye, but may spread easily to the fellow eye.
Bacterial conjunctivitis due to the common pyogenic (pus-producing) bacteria causes marked grittiness/irritation and a stringy, opaque, grey or yellowish mucopurulent discharge (gowl, goop, sleep, or other regional names) that may cause the lids to stick together (matting), especially after sleeping. Another symptom that could be caused by Bacterial Conjunctivitis is severe crusting of the infected eye and the surrounding skin. However discharge is not essential to the diagnosis, contrary to popular belief. Many other bacteria (e.g., Chlamydia, Moraxella) can cause a non-exudative but very persistent conjunctivitis without much redness. The gritty and/or scratchy feeling is sometimes localised enough for patients to insist they must have a foreign body in the eye. The more acute pyogenic infections can be painful. Like viral conjunctivitis, it usually affects only one eye but may spread easily to the other eye.
Irritant or toxic conjunctivitis is irritable or painful when the infected eye is pointed far down or far up. Discharge and itch are usually absent. This is the only group in which severe pain may occur.

Signs :

One eye with conjunctivitis.
Infection (redness) conjunctiva on one or both eyes should be apparent, but may be quite mild. Except in obvious pyogenic or toxic/chemical conjunctivitis, a slit lamp (biomicroscope) is needed to have any confidence in the diagnosis. Examination of the tarsal conjunctiva is usually more diagnostic than the bulbar conjunctiva.
Allergic conjunctivitis shows pale watery swelling or edema of the conjunctiva and sometimes the whole eyelid, often with a ropy, non-purulent mucoid discharge. There is variable redness. Viral conjunctivitis, commonly known as "pink eye", shows a fine diffuse pinkness of the conjunctiva which is easily mistaken for the 'ciliary infection' of iritis, but there are usually corroborative signs on biomicroscopy, particularly numerous lymphoid follicles on the tarsal conjunctiva, and sometimes a punctate keratitis.
Pyogenic bacterial conjunctivitis shows an opaque purulent discharge, a very red eye, and on biomicroscopy there are numerous white cells and desquamated epithelial cells seen in the 'tear gutter' along the lid margin. The tarsal conjunctiva is a velvety red and not particularly follicular. Non-pyogenic infections can show just mild injection and be difficult to diagnose. Scarring of the tarsal conjunctiva is occasionally seen in chronic infections, especially in trachoma.
Irritant or toxic conjunctivitis show primarily marked redness. If due to splash injury, it is often present only in the lower conjunctival sac. With some chemicals—above all with caustic alkalis such as sodium hydroxide—there may be necrosis of the conjunctiva with a deceptively white eye due to vascular closure, followed by sloughing of the dead epithelium. This is likely to be associated with slit-lamp evidence of anterior uveitis.

Differential diagnosis :

Conjunctivitis symptoms and signs are relatively non-specific. Even after biomicrosopy, laboratory tests are often necessary if proof of aetiology is needed.
A purulent discharge strongly suggests bacterial cause, unless there is known exposure to toxins. Infection with Neisseria gonorrhoeae should be suspected if the discharge is particularly thick and copious.
A diffuse, less "injected" conjunctivitis (looking pink rather than red) suggests a viral cause, especially if numerous follicles are present on the lower tarsal conjunctiva on biomicroscopy.
Scarring of the tarsal conjunctiva suggests trachoma, especially if seen in endemic areas, if the scarring is linear (von Arlt's line), or if there is also corneal vascularisation.
Clinical tests for lagophthalmos, dry eye (Schirmer test) and unstable tear film may help distinguish the various types of dry eye.
Other symptoms including pain, blurring of vision and photophobia should not be prominent in conjunctivitis. Fluctuating blurring is common, due to tearing and mucoid discharge. Mild photophobia is common. However, if any of these symptoms are prominent, it is important to exclude other diseases such as glaucoma, uveitis, keratitis and even meningitis or caroticocavernous fistula.

Investigations :

These are done infrequently because most cases of conjunctivitis are treated empirically and (eventually) successfully, but often only after running the gamut of the common possibilities.
Swabs for bacterial culture are necessary if the history & signs suggest bacterial conjunctivitis, but there is no response to topical

antibiotics. Research studies indicate that many bacteria implicated in low-grade conjunctivitis are not detected by the usual culture methods of medical microbiology labs, so negative results are common. Viral culture may be appropriate in epidemic case clusters. Conjunctival scrapes for cytology can be useful in detecting chlamydial and fungal infections, allergy and dysplasia, but are rarely done because of the cost and the general lack of laboratory staff experienced in handling ocular specimens. Conjunctival incisional biopsy is occasionally done when granulomatous diseases (e.g., sarcoidosis) or dysplasia are suspected.

Treatment and management :

Conjunctivitis sometimes requires medical attention. The appropriate treatment depends on the cause of the problem. For the allergic type, cool compresses and artificial tears sometimes relieve discomfort in mild cases. In more severe cases, non-steroidal anti-inflammatory medications and antihistamines may be prescribed. Some patients with persistent allergic conjunctivitis may also require topical steroid drops.
Bacterial conjunctivitis is usually treated with antibiotic eye drops or ointments that cover a broad range of bacteria (chloramphenicol or fusidic acid used in UK). However evidence suggests that this does not affect symptom severity and gains only modest reduction in duration from an average of 4.8 days (untreated controls) to 3.3 days for those given immediate antibiotics. Deferring antibiotics yields almost the same duration as those immediately starting treatment with 3.9 days duration, but with half the two-week clinic reattendance rate.
Although there is no cure for viral conjunctivitis, symptomatic relief may be achieved with cool compresses and artificial tears. For the worst cases, topical corticosteroid drops may be prescribed to reduce the discomfort from inflammation. However prolonged usage of corticosteroid drops increases the risk of side effects. Antibiotic drops may also be used for treatment of complimentary infections. Patients are often advised to avoid touching their eyes or sharing towels and washcloths. Viral conjunctivitis usually resolves within 3 weeks.However in worst cases it may take over a month.
Conjunctivitis due to burns, toxic and chemical require careful wash-out with saline, especially beneath the lids, and may require topical steroids. The more acute chemical injuries are medical emergencies, particularly alkali burns, which can lead to severe scarring, intraocular damage or even loss of the eye. Fortunately, such injuries are uncommon.

BREAST CANCER

2007-09-15T19:57:00.000+05:30

Breast cancer is a cancer of the glandular breast tissue.
Worldwide, breast cancer is the fifth most common cause of cancer death (after lung cancer, stomach cancer, liver cancer, and colon cancer). In 2005, breast cancer caused 502,000 deaths (7% of cancer deaths; almost 1% of all deaths) worldwide. Among women worldwide, breast cancer is the most common cancer and the most common cause of cancer death.
In the United States, breast cancer is the third most common cause of cancer death (after lung cancer and colon cancer). In 2007, breast cancer is expected to cause 40,910 deaths (7% of cancer deaths; almost 2% of all deaths) in the U.S.[2Among women in the U.S., breast cancer is the most common cancer and the second most common cause of cancer death (after lung cancer). Women in the U.S. have a 1 in 8 lifetime chance of developing invasive breast cancer and a 1 in 33 chance of breast cancer causing their death
The number of cases has significantly increased since the 1970s, a phenomenon partly blamed on modern lifestyles in the Western world.

Contents
1 History
2 Classification
2.1 Histologic types
2.1.1 Carcinomas
2.1.1.1 in situ
2.1.1.2 Invasive
2.1.2 Sarcomas
2.2 Clinical categorizations
3 Symptoms
4 Epidemiologic risk factors and etiology
4.1 Age
4.2 Sex
4.3 Heredity
4.4 Diet
4.5 Alcohol
4.6 Obesity
4.7 Hormones
4.8 Environmental causes
4.8.1 Tobacco
4.8.2 Radiation
4.8.3 Impact of environmental estrogenic mimics
4.8.4 Dioxins
4.8.5 Light levels
4.9 Viral breast cancer pathogenesis research
4.10 Factors with minimal or no impact on breast cancer risk
4.10.1 Abortion
4.10.2 Deodorants
4.10.3 Fertility treatments
4.10.4 Phytoestrogens and soy
5 Prevention in high-risk individuals
5.1 Prophylactic oophorectomy
5.2 Prophylactic mastectomy
5.3 Medications
5.3.1 Selective estrogen receptor modulators (SERMs)
6 Screening
6.1 X-ray mammography
6.2 Criticisms of screening mammography
6.2.1 Mammography in women less than 50 years old
6.3 Enhancements to mammography
6.4 Breast MRI
6.5 Breast ultrasound
6.6 Breast self-exam
6.7 BRCA testing
7 Diagnosis
8 Staging
9 Treatment personalization with gene expression profiling
10 Treatment
10.1 Surgery
10.2 Radiation therapy
10.2.1 Indications for radiation
10.2.2 Types of radiotherapy
10.2.3 Side effects of radiation therapy
10.3 Systemic therapy
10.3.1 Chemotherapy
10.3.2 Hormonal treatment
10.3.3 Targeted therapy
10.3.4 Antiangiogenic therapy
10.3.5 Preclinical
10.3.5.1 Protein tyrosine phosphatase 1B (PTP1B)
10.3.5.2 Flax seeds
10.3.5.3 Evista
10.3.6 Traditional Chinese medicine
11 Psychological aspects of breast cancer diagnosis and treatment
12 Prognosis
13 Breast cancer in males
14 Breast cancer metastasis
15 Breast cancer awareness
16 See also
17 References
18 External links
18.1 General
18.2 Research and statistics
18.3 Clinical
18.4 Videos
18.5 Other

C-T Scan - a diagnostic breakthrough

2007-09-14T18:19:00.000+05:30

Computed tomography (CT), originally known as computed axial tomography (CAT or CT scan) and body section roentgenography, is a medical imaging method employing tomography where digital geometry processing is used to generate a three-dimensional image of the internals of an object from a large series of two-dimensional X-ray images taken around a single axis of rotation. The word "tomography" is derived from the Greek tomos (slice) and graphein (to write). CT produces a volume of data which can be manipulated, through a process known as windowing, in order to demonstrate various structures based on their ability to block the X-ray beam. Although historically (see below) the images generated were in the axial or transverse plane (orthogonal to the long axis of the body), modern scanners allow this volume of data to be reformatted in various planes or even as volumetric (3D) representations of structures.

History
The first commercially viable CT scanner was invented by Godfrey Newbold Hounsfield in Hayes, England at Thorn EMI Central Research Laboratories using X-rays. Hounsfield conceived his idea in 1967, and it was publicly announced in 1972. It is claimed that the CT scanner was "the greatest legacy" of the Beatles; the massive profits from their record sales enabled EMI to fund scientific research.[1] Allan McLeod Cormack of Tufts University, Massachusetts, USA independently invented a similar process and they shared a Nobel Prize in medicine in 1979.

The prototype CT scanner
The original 1971 prototype took 160 parallel readings through 180 angles, each 1° apart, with each scan taking a little over five minutes. The images from these scans took 2.5 hours to be processed by algebraic reconstruction techniques on a large computer.
The first production X-ray CT machine (called the EMI-Scanner) was limited to making tomographic sections of the brain, but acquired the image data in about 4 minutes (scanning two adjacent slices) and the computation time (using a Data General Nova minicomputer) was about 7 minutes per picture. This scanner required the use of a water-filled Perspex tank with a pre-shaped rubber "head-cap" at the front, which enclosed the patient's head. The water-tank was used to reduce the dynamic range of the radiation reaching the detectors (between scanning outside the head compared with scanning through the bone of the skull). The images were relatively low resolution, being composed of a matrix of only 80 x 80 pixels. The first EMI-Scanner was installed in Atkinson Morley's Hospital in Wimbledon, England, and the first patient brain-scan was made with it in 1972.

a historic EMI-Scanner
In the U.S., the first installation was at the Mayo Clinic. As a tribute to the impact of this system on medical imaging the Mayo Clinic has an EMI scanner on display in the Radiology Department.
The first CT system that could make images of any part of the body, and did not require the "water tank" was the ACTA scanner designed by Robert S. Ledley, DDS at Georgetown University.

can u understand a doctor's writing

2007-09-14T17:14:00.000+05:30

Why do Doctors Write so BADLY?!!

Writing badly for a doctor is a matter of survival! In a single eight hour shift s/he can write their signature alone fifty or more times!
The real problem is the amount of paperwork that needs to be done for each patient. For legal reasons, everything done, or found, has to be documented on paper prior to discharge. Many doctors eventually realize that most of this.
paper-trail ends up stuffed in files and forgotten, and interferes in what is really important - seeing and treating patients.
Many also realize that what they write is not intended for the public to read, only for themselves and their peers, and as you'll see, the way we write is decipherable amongst ourselves once you know what to look for. Also you'll see that bad handwriting in doctors is made not born (how could anyone get through college far less med school writing so badly).

How to Write like a Doctor
Abbreviate - It's much faster to write 'SOB' than 'shortness of breath'.
Write small - distance takes time so writing in between letters small saves time.
Skip vowels - cn u rd ths sntnce? Most sentences can be read without vowels.
Write the first two or three letters legibly then scrawl - as doctors and allied health pros use the same words over and over it only takes one or two letters in context to recognize a specialist word

Diabetes - a human curse

2007-09-14T16:45:00.000+05:30

What is diabetes?

Diabetes happens when the body cannot make or use insulin correctly. Insulin is a hormone that turns the sugars in the foods we eat into energy. When a person has diabetes, too much sugar stays in the blood. This can damage different parts of the body, including the heart, blood vessels, eyes, nerves and kidneys. There are a few different types of diabetes:

Type 1: The body cannot make insulin. It is also called “juvenile diabetes”.

Type 2: The body cannot use the insulin that it makes, or the insulin that it makes does not work correctly. Gestational: Diabetes during pregnancy.
The good news is that diabetes can often be prevented by healthy habits like a good diet and exercise. If someone already has diabetes, he or she can learn to control it and reduce the risk of complications.

Who is at risk?
Anyone can develop diabetes, but some people are more at risk than others. You are at greater risk for diabetes if you:
Are over 45 years old.
Are overweight.
Are African American, Hispanic/Latino, Asian, Pacific Islander or American Indian.
Have a family history of diabetes.
Have high cholesterol.
Have had gestational diabetes during pregnancy.
Have given birth to a baby that weighed more than 9 lbs.
Exercise less than 3 times a week.
While you cannot change some of these factors, you can change others. For example, you cannot change your age, but you can exercise more often. These kinds of changes will help reduce your risk of developing diabetes.

How will I know if I have diabetes?

Diabetes often has no symptoms or warning signs. The only way to be sure is to have your blood tested for glucose (blood sugar). If symptoms do appear, they might include:
Feeling tired
Feeling irritable
Urinating more than normal
Being very thirsty
Being very hungry
Unexplained weight loss
Blurred vision
If you are experiencing some of these symptoms or think that you might be at risk for diabetes, be sure to talk to your doctor about getting tested.

What can I do to prevent diabetes?

Healthy eating and exercise habits are the best way to prevent diabetes. These are also great ways to help keep diabetes in control if you already have it.
To eat healthy, pick foods that are nutrient-rich. This means that they have many vitamins, but not much fat or sugar. When it comes to foods that are high in sugar, like ice cream or cookies, make sure that you are not overeating. You can still eat these foods, but eat them in moderation.
Exercising three or four times a week is another way to lower your risk of developing diabetes. For example, you might go for walks, run, bike, swim, join a local sports team or try a dance class. The key here is to start small and find something that you enjoy.

What if I already have diabetes?

If you already have diabetes, you can lessen your chance of developing kidney disease by keeping your blood sugar under control. Some ways to do this are to:
Check your blood sugar often.
Ask your doctor about a blood test called “hemoglobin A1C.” This tests how your normal blood sugars have been over the past 2 or 3 months. It is a kind of “report card” for your blood sugar.
Follow your doctor’s advice about insulin injections, medicines, diet and exercise.
You can also reduce your risk for kidney failure if you:
Monitor your blood pressure. If your blood pressure is high, talk to your doctor about taking an ACE inhibitor.
Have your doctor check your urine for protein.
Ask your doctor to calculate your eGFR (estimated glomerular filtration rate). This number is based on the creatinine level in your blood, as well as your age, sex and race.

HYPERTENSION - an overview

2007-09-14T12:11:00.000+05:30

Background for Hypertensive diseeases

Uncontrolled and prolonged elevation of blood pressure (BP) can lead to a variety of changes in the myocardial structure, coronary vasculature, and conduction system of the heart. These changes can lead to the development of left ventricular hypertrophy (LVH), coronary artery disease, various conduction system diseases, and systolic and diastolic dysfunction of the myocardium, which manifest clinically as angina or myocardial infarction, cardiac arrhythmias (especially atrial fibrillation), and congestive heart failure (CHF). Thus, hypertensive heart disease is a term applied generally to heart diseases, such as LVH, coronary artery disease, cardiac arrhythmias, and CHF, caused by direct or indirect effects of elevated BP. Although these diseases generally develop in response to chronically elevated BP, marked and acute elevation of BP can also lead to accentuation of an underlying predisposition to any of the symptoms traditionally associated with chronic hypertension.

PathophysiologyThe pathophysiology of hypertensive heart disease is a complex interplay of various hemodynamic, structural, neuroendocrine, cellular, and molecular factors. On one hand, these factors play integral roles in the development of hypertension and its complications; on the other hand, elevated BP itself can modulate these factors. Elevated BP leads to adverse changes in cardiac structure and function in 2 ways: directly by increased afterload and indirectly by associated neurohormonal and vascular changes. Elevated 24-hour ambulatory BP and nocturnal BP have been demonstrated to be more closely related to various cardiac pathologies, especially in African Americans. The pathophysiologies of the various cardiac effects of hypertension differ and are described in this section.

Left ventricular hypertrophy

Of patients with hypertension, 15-20% develop LVH. The risk of LVH is increased 2-fold by associated obesity. The prevalence of LVH based on ECG findings, which are not a sensitive marker at the time of diagnosis of hypertension, is variable. Studies have shown a direct relationship between the level and duration of elevated BP and LVH.
LVH, defined as an increase in the mass of the left ventricle (LV), is caused by the response of myocytes to various stimuli accompanying elevated BP. Myocyte hypertrophy can occur as a compensatory response to increased afterload. Mechanical and neurohormonal stimuli accompanying hypertension can lead to activation of myocardial cell growth, gene expression (Some of the genes are given expression primarily in fetal cardiomyocytes.), and, thus, LVH. In addition, activation of the renin-angiotensin system, through the action of angiotensin II on angiotensin I receptors, leads to growth of interstitium and cell matrix components. Thus, the development of LVH is characterized by myocyte hypertrophy and by an imbalance between the myocytes and the interstitium of the myocardial skeletal structure.
Various patterns of LVH have been described, including concentric remodeling, concentric LVH, and eccentric LVH. Concentric LVH is an increase in LV thickness and LV mass with increased LV diastolic pressure and volume, commonly observed in persons with hypertension. Compare this with eccentric LVH, in which LV thickness is increased not uniformly but at certain sites, such as the septum. Concentric LVH is a marker of poor prognosis in the presence of hypertension. While the development of LVH initially plays a protective role in response to increased wall stress to maintain adequate cardiac output, later it leads to the development of diastolic and, ultimately, systolic myocardial dysfunction.

Left atrial abnormalities

Frequently underappreciated, structural and functional changes of the left atrium (LA) are very common in patients with hypertension. The increased afterload imposed on the LA by the elevated LV end-diastolic pressure secondary to increased BP leads to impairment of the LA and LA appendage function plus increased LA size and thickness. Increased LA size accompanying hypertension in the absence of valvular heart disease or systolic dysfunction usually implies chronicity of hypertension and may correlate with the severity of LV diastolic dysfunction. In addition to these structural changes, these patients are predisposed to atrial fibrillation. Atrial fibrillation, with loss of atrial contribution in the presence of diastolic dysfunction, may precipitate overt heart failure.

Valvular disease

Although valvular disease does not cause hypertensive heart disease, chronic and severe hypertension can cause aortic root dilatation, leading to significant aortic insufficiency. Some degree of hemodynamically insignificant aortic insufficiency is often found in patients with uncontrolled hypertension. An acute rise in BP may accentuate the degree of aortic insufficiency, with return to baseline when BP is better controlled. In addition to causing aortic regurgitation, hypertension is also thought to accelerate the process of aortic sclerosis and cause mitral regurgitation.

Heart failure

Heart failure is a common complication of chronically elevated BP. Hypertension as a cause of CHF is frequently underrecognized, partly because at the time heart failure develops, the dysfunctioning LV is unable to generate the high BP, thus obscuring the etiology of the heart failure. The prevalence of asymptomatic diastolic dysfunction in patients with hypertension and without LVH may be as high as 33%. Chronically elevated afterload and resulting LVH can adversely affect both the active early relaxation phase and late compliance phase of ventricular diastole.
Diastolic dysfunction is common in persons with hypertension. It is usually, but not invariably, accompanied by LVH. In addition to elevated afterload, other factors that may contribute to the development of diastolic dysfunction include coexistent coronary artery disease, aging, systolic dysfunction, and structural abnormalities such as fibrosis and LVH. Asymptomatic systolic dysfunction usually follows. Later in the course of disease, the LVH fails to compensate by increasing cardiac output in the face of elevated BP and the left ventricular cavity begins to dilate to maintain cardiac output. As the disease enters the end stage, LV systolic function decreases further. This leads to further increases in activation of the neurohormonal and renin-angiotensin systems, leading to increases in salt and water retention and increased peripheral vasoconstriction, eventually overwhelming the already compromised LV and progressing to the stage of symptomatic systolic dysfunction.
Apoptosis, or programmed cell death, stimulated by myocyte hypertrophy and the imbalance between its stimulants and inhibitors, is considered to play an important part in the transition from compensated to decompensated stage. The patient may become symptomatic during the asymptomatic stages of the LV systolic or diastolic dysfunction, owing to changes in afterload conditions or to the presence of other insults to the myocardium (eg, ischemia, infarction). A sudden increase in BP can lead to acute pulmonary edema without necessarily changing the LV ejection fraction. Generally, development of asymptomatic or symptomatic LV dilatation or dysfunction heralds rapid deterioration in clinical status and markedly increased risk of death. In addition to LV dysfunction, right ventricular thickening and diastolic dysfunction also develop as results of septal thickening and LV dysfunction.

Myocardial ischemia

Patients with angina have a high prevalence of hypertension. Hypertension is an established risk factor for the development of coronary artery disease, almost doubling the risk. The development of ischemia in patients with hypertension is multifactorial.
Importantly, in patients with hypertension, angina can occur in the absence of epicardial coronary artery disease. The reason is 2-fold. Increased afterload secondary to hypertension leads to an increase in left ventricular wall tension and transmural pressure, compromising coronary blood flow during diastole. In addition, the microvasculature, beyond the epicardial coronary arteries, has been shown to be dysfunctional in patients with hypertension and it may be unable to compensate for increased metabolic and oxygen demand.
The development and progression of arteriosclerosis, the hallmark of coronary artery disease, is exacerbated in arteries subjected to chronically elevated BP. Shear stress associated with hypertension and the resulting endothelial dysfunction causes impairment in the synthesis and release of the potent vasodilator nitric oxide. A decreased nitric oxide level promotes the development and acceleration of arteriosclerosis and plaque formation. Morphologic features of the plaque are identical to those observed in patients without hypertension.

Cardiac arrhythmias

Cardiac arrhythmias commonly observed in patients with hypertension include atrial fibrillation, premature ventricular contractions, and ventricular tachycardia.
The risk of sudden cardiac death is increased. Various mechanisms thought to play a part in the pathogenesis of arrhythmias include altered cellular structure and metabolism, inhomogeneity of the myocardium, poor perfusion, myocardial fibrosis, and fluctuation in afterload. All of these may lead to an increased risk of ventricular tachyarrhythmias.
Atrial fibrillation (paroxysmal, chronic recurrent, or chronic persistent) is observed frequently in patients with hypertension. In fact, elevated BP is the most common cause of atrial fibrillation in the Western hemisphere. In one study, nearly 50% of patients with atrial fibrillation had hypertension. Although the exact etiology is not known, left atrial structural abnormalities, associated coronary artery disease, and LVH have been suggested as possible contributing factors. The development of atrial fibrillation can cause decompensation of systolic and, more importantly, diastolic dysfunction, owing to loss of atrial kick, and it also increases the risk of thromboembolic complications, most notably stroke.
Premature ventricular contractions, ventricular arrhythmias, and sudden cardiac death are observed more often in patients with LVH than in those without LVH. The etiology of these arrhythmias is thought to be concomitant coronary artery disease and myocardial fibrosis

Race

In the United States, hypertension is more prevalent in African Americans than in whites, as is death from hypertensive heart disease. This difference is attributed to factors other than race because the prevalence of hypertension among African Americans and whites is the same in the United Kingdom and because hypertension is not very common on the African continent. In addition, hypertension is the most common etiology of heart failure in African Americans in the United States.
Sex

Systolic BP increases with age. This increase is more marked in men until women reach menopause, when BP rises more sharply in women and reaches levels higher than in men. The prevalence of hypertension is higher in men younger than 55 years but is higher in women older than 55 years. The prevalence of hypertensive heart disease probably follows the same pattern.
Age

BP increases with age, as does the prevalence of hypertensive heart disease, which is affected by the severity of BP increase.
HistorySymptoms of hypertensive heart disease depend on the duration, severity, and type of disease. In addition, the patient may or may not be aware of the diagnosis of hypertension.
Left ventricular hypertrophy: Patients with LVH alone are totally asymptomatic unless the LVH leads to the development of diastolic dysfunction and heart failure.

Heart failure
Although symptomatic diastolic heart failure and systolic heart failure are indistinguishable, the clinical history may be quite revealing. In particular, individuals who abruptly develop severe symptoms of CHF and rapidly return to baseline with medical therapy are more likely to have isolated diastolic dysfunction.

Heart failure symptoms include the following:
Exertional and nonexertional dyspnea (NYHA classes I-IV)
Orthopnea
Paroxysmal nocturnal dyspnea
Fatigue (more common in systolic dysfunction)
Ankle edema and weight gain
Abdominal pain secondary to congested, distended liver
Altered mentation in severe cases
Patients can present with acute pulmonary edema due to sudden decompensation in LV systolic or diastolic dysfunction caused by precipitating factors such as acute rise in BP, dietary indiscretion, or myocardial ischemia. Patients can develop cardiac arrhythmias, especially atrial fibrillation, or they can develop symptoms of heart failure insidiously over time.
Myocardial ischemia
Angina, a frequent complication of hypertensive heart disease, is also indistinguishable from other causes of myocardial ischemia.
Typical symptoms of angina include substernal chest pain lasting less than 20 minutes (versus >20 min in infarction). Pain is described in the following ways:
Heaviness, pressure, squeezing
Radiating to neck, jaw, upper back, or left arm
Provoked by emotional or physical exertion
Relieved with rest or sublingual nitroglycerin
Patients also may present with atypical symptoms without chest pain, such as exertional dyspnea, commonly referred to as an angina equivalent.
The patient may present with chronic stable angina or acute coronary syndrome, including myocardial infarction without ST-segment elevation and acute myocardial infarction with ST elevation. Ischemic ECG changes may be found in individuals presenting with hypertensive crisis in whom no significant coronary atherosclerosis is detectable by coronary angiography.
Acute coronary symptoms can be precipitated by a ruptured atherosclerotic plaque or by an acute and severe rise in BP leading to a sudden increase in transmural pressure without a change in stability of the plaque.
Cardiac arrhythmias: These can cause a variety of symptoms, including palpitations, near or total syncope, precipitation of angina, sudden cardiac death, and precipitation of heart failure, especially with atrial fibrillation in diastolic dysfunction.

Physical

Physical signs of hypertensive heart disease depend on the predominant cardiac abnormality and the duration and severity of the hypertensive heart disease. Findings from the physical examination may be entirely normal in the very early stages of the disease, or the patient may have classic signs upon examination. In addition to generalized findings attributable directly to high BP, the physical examination may reveal clues to a potential etiology of hypertension, such as truncal obesity and striae in Cushing syndrome, renal artery bruit in renal artery stenosis, and abdominal mass in polycystic kidney disease.
Pulses: The arterial pulses are normal in the early stages of the disease.
Rhythm
Regular if the patient is in sinus rhythm
Irregularly irregular if the patient is in atrial fibrillation
Rate
Normal in patients in sinus rhythm and not in decompensated heart failure
Tachycardic in patients with heart failure and in patients with atrial fibrillation and a rapid ventricular response
Volume
Normal
Decreased in patients with LV dysfunction
Additional findings -

May include radial-femoral delay if the etiology of hypertension is coarctation of the aorta

Blood pressure: Systolic and/or diastolic BP is elevated (>140/90 mm Hg). Mean BP and pulse pressure generally are also elevated. The BP in the upper extremities may be higher than that in the lower extremities in patients with coarctation of the aorta. BP may be normal at the time of evaluation if the patient is on adequate antihypertensive medications or the patient has advanced LV dysfunction and the LV cannot generate enough stroke volume and cardiac output to produce an elevated BP.

Veins: In patients with heart failure, jugular veins may be distended; the predominant waves depend on the severity of the heart failure and any other associated lesions.

Heart
Apex: The apical impulse is sustained and nondisplaced in patients without significant systolic LV dysfunction but with LVH. A presystolic S4 may be felt. Later in the course of disease, when significant systolic LV dysfunction supervenes, the apical impulse is displaced laterally, owing to LV dilatation.
Right ventricle: A lift is present late in the course of heart failure if significant pulmonary hypertension develops.
Heart sounds: S1 is normal in intensity and character. S2 at the right upper sternal border is loud because of an accentuated aortic component (A2); it can have a reverse or paradoxical split due either to increased afterload or to associated left bundle-branch block (LBBB). S4 frequently is palpable and audible, implying the presence of a stiffened, noncompliant ventricle due to chronic pressure overload and LVH. S3 typically is not present initially but is audible in the presence of heart failure, either systolic or diastolic.
Murmurs: An early decrescendo diastolic murmur of aortic insufficiency may be heard along the mid-to-left parasternal area, especially in the presence of acutely elevated BP, frequently disappearing once the BP is better controlled. In addition, an early to mid systolic murmur of aortic sclerosis is commonly audible. A holosystolic murmur of mitral regurgitation may be present in patients with advanced heart failure and dilated mitral annulus.
Lungs: Findings upon chest examination may be normal or may include signs of pulmonary congestion, such as rales, decreased breath sounds, and dullness to percussion due to pleural effusion.
Abdomen: Abdominal examination may reveal a renal artery bruit in patients with hypertension secondary to renal artery stenosis, a pulsatile expansile mass of abdominal aortic aneurysm, and hepatomegaly and ascites due to CHF.
Extremities: Ankle edema may be present in patients with advanced heart failure.
CNS and retina
CNS examination findings are usually unremarkable unless the patient has had previous cerebrovascular accidents with residual deficit.
Examination of the fundi may reveal evidence of hypertensive retinopathy, the severity of which depends on the duration and severity of hypertension, or earlier signs of hypertension such as arteriovenous nicking.

causes

cause of hypertensive heart disease is chronically elevated BP. The causes of elevated BP are diverse. In adults, the following causes should be considered:
Essential hypertension accounts for 90% of cases of hypertension in adults.
Secondary causes of hypertension account for the remaining 10% of cases of chronically elevated BP. These include the following:
Renal causes
Renal artery stenosis
Polycystic kidney disease
Chronic renal failure
Intrarenal Vasculitis
Endocrine causes
Primary hyperaldosteronism
Pheochromocytoma
Cushing syndrome
Congenital adrenal hyperplasia
Hypothyroidism and hyperthyroidism
Acromegaly
Exogenous hormone (eg, corticosteroids, estrogens), sympathomimetics, monoamine oxidase inhibitors (MAOIs), and tyramine-containing foods
Others
Coarctation of aorta
Raised intracranial pressure
Sleep apnea
Isolated systolic hypertension - Can be observed in elderly people, due to increased stiffness of the vasculature
Isolated systolic hypertension - Can be observed in thyrotoxicosis, atrioventricular (AV) fistula, aortic regurgitation, beriberi, Paget disease, and patent ductus arteriosus (ie, due to increase cardiac output secondary to a hyperdynamic circulation)

DIABETIC FOOT-POST OPERATIVE

2007-09-02T20:44:00.000+05:30

Diabetic Foot

If a doctor has ever said you had an elevated blood sugar level - even just once when you were pregnant - you are at risk for diabetes. About 15.7 million people (5.9 percent of the United States population) have the disease. Nervous system impairment (neuropathy) is a major complication that may cause you to lose feeling in your feet or hands. This means you won't know right away if you hurt yourself. The problem affects about 60 to 70 percent of people with diabetes.

Here's some basic advice for taking care of your feet:

Wash your feet every day with mild soap and warm water. Test the water temperature with your hand first. Don't soak your feet. When drying them, pat each foot with a towel and be careful between your toes.
Use quality lotion to keep the skin of your feet soft and moist - but don't put any lotion between your toes.
Trim your toe nails straight across. Avoid cutting the corners. Use a nail file or emery board. If you find an ingrown toenail, see your doctor.
Don't use antiseptic solutions, drugstore medications, heating pads or sharp instruments on your feet. Don't put your feet on radiators or in front of the fireplace.
Always keep your feet warm. Wear loose socks to bed. Don't get your feet wet in snow or rain. Wear warm socks and shoes in winter.
Don't smoke or sit cross-legged. Both decrease blood supply to your feet.

Basic life saving techniques

2007-09-02T20:20:00.000+05:30

Mouth-to-Mouth Resuscitation

Mouth-to-Mouth-and-Nose Resuscitation on a Child Under Age 8 or on an Infant

1. Place the child on a hard, flat surface.
2 .Look into the mouth and throat to ensure that the airway is clear. If an object is present, try to sweep it out with your fingers. If unsuccessful and the object is blocking the airway, apply the Heimlich maneuver (see p. 1205). If vomiting occurs, turn the child onto his or her side and sweep out the mouth with two fingers.
3. Tilt the head back slightly to open the airway.

4. Place your mouth tightly over the nose and mouth. Blow two quick, shallow breaths (smaller breaths than you would give to an adult). Watch for the chest to rise.
5. Remove your mouth. Look for the chest to fall as the child exhales.
6. Listen for the sounds of breathing. Feel for the child’s breath on your cheek. If breathing does not start on its own, repeat the procedure.

Mouth-to-Mouth Resuscitation on a Child Age 8 or Older or on an Adult

1. Make sure the person is lying on a hard, flat surface. Look into the mouth and throat to ensure that the airway is clear. If an object is present, try to sweep it out with your fingers (wear disposable surgical gloves if they are available). Apply the Heimlich maneuver (see p. 1205) if unsuccessful and the object is blocking the airway. If vomiting occurs, turn the person on his or her side and sweep out the mouth with two fingers. Do not place your finger in the mouth if the person is rigid or is having a seizure.

2. Tilt the head back slightly to open the airway. Put upward pressure on the jaw to pull it forward.

3. Pinch the nostrils closed with thumb and index finger. Place your mouth tightly over the person’s mouth. Use a mouthpiece if one is available. Blow two quick breaths and watch for the person’s chest to rise.

4. Release the nostrils. Look for the person’s chest to fall as he or she exhales. Listen for the sounds of breathing. Feel for the person’s breath on your cheek. If the person does not start breathing on his or her own, repeat the procedure.

Blood Types Can Be Converted; May End Shortages

2007-09-01T18:53:00.000+05:30

Blood types A, B, and AB can be efficiently converted to type O, which is safe to give to anyone, says an international team of researchers.
The scientists identified bacterial proteins that can quickly convert one blood type to another by clipping away sugar molecules on red blood cells.The find may create a universally safe supply of blood and may help end shortages, since mismatched blood transfusions can quickly cause death.

Deadly Mismatches

Under the ABO system discovered in 1900, blood is classified into four groups based on the presence or absence of complex sugar molecules on the surfaces of red blood cells.
"Group A has an enzyme that puts a sugar molecule on the end," explained Geoffrey Daniels, a transfusion scientist at the University of Bristol in England.
"Group B also has an extra sugar molecule, different from that on group A, at the end of its structure," he added. "But group O has neither kind of sugar molecule."
People naturally create antibodies to the sugars they lack. So people with blood type A naturally have antibodies to the blood plasma from type B, and vice versa.
If people get blood transfusions of the wrong type, their antibodies attack the foreign sugars, mounting a vigorous and oftentimes deadly immune response.
"The blood cells clump together as a consequence of the antibodies acting like a glue between cells, and thus blood gets very thick," said Steve Withers, a bioorganic chemist at the University of British Columbia, Canada.
"The red blood cells can explode."

Protein Clippers :-

One way to solve the supply crunch is to snip away the sugar molecule in the A and B groups, giving antibodies no targets, said Henrik Clausen, a sugar biologist at the University of Copenhagen in Denmark.
Researchers elsewhere had demonstrated this could be done. But Clausen and his colleagues looked at hundreds of different bacteria for enzymes that could do the task much more efficiently.
"Think of the sugar molecules attached to a blood cell as a string of pearls," Clausen said.
"We carefully clipped away one pearl that was the 'A' and 'B' in the blood groups A, B, and AB, making the blood acceptable to all recipients," he added.
"The process may help address the current blood shortage."

Blood Supply

The method is useful in generating the type of blood from groups A and B that will help all recipients when there is a shortage in blood supply, said the University of Bristol's Daniels.
"On a more immediate level, it will help patients who need regular transfusions, and specifically require blood from group O."
According to study leader Clausen, "accidental transfusion of the wrong type of blood has a higher risk of death than infectious disease.
"This method makes blood transfusion more safe."

ABDOMINAL DISTENSION

2007-08-26T19:35:00.000+05:30

5 F for abdominal distention.

Flatus .
Fetus .
Faeces .
Fat .
Fluid .

HEART SOUNDS

2007-08-26T14:53:00.000+05:30

HEART SOUNDS

Heart sounds ( FOUR ) are normally produced within the heart during cardiac cycle.The main cause seems to be either acceleration or deceleration of blood flow and closure of the valves। Among them 1st & 2nd heartsounds can be heard nicely by placing stethescope on chest but all the four sounds can be recorded by phonocardiograph। The 3rd heart sound sometimes may be heard in normal individual। The 4th sound is never heard in normal heart. In some diseased state all four heart sounds may be heard.

1st HEART SOUND :- It is heard at the onset of ventricularsystole during closure of the A-V valves. It'sduration is longer ( 0.15 sec ) and it's frequency islower ( 25-45 Hz ) then the 2nd heart sound.1st heartcound can be heard on all the areas of the chest butbest heard over mitral area. It sounds like the word " LUBB ".

2ND HEART SOUND :- It is heard during isovolumetric relaxation ofventricles ( diastoles ) mainly due to closure ofsemilunar valves. The period between the 1st and the2nd heart sound is the clinical systole. It is ofshorter duration ( 0.12 sex ) and is of higherfrequency ( more then 50 Hz ) then the 1st heartsound. 2nd heart sound can also be heard on all theareas of the chest but heard best over aortic area. Itsounds like the word " DUPP ".

3RD HEART SOUND :- It is low pitched soft sound of 0.1 sec duration,heard in the early diastle and is produced due torapid filling phase i.e after the 2nd heart sound. Itoccurs probably due to vibration in the ventricularwall caused by movement of blood. It can be heardsometimes in normal individuals with thin chest andhigh venous return. Third sound in abnormal situationsignifies heart failure etc. It is best heard at theapical area.

4TH HEART SOUND :- It is also called atrial sound and is produced during atrial contraction. It is heard just before the 1stheart sound i.e late in the diastole. It is beleivedto be produced when the atria are forcefully trying topump blood in non-complaint( stiff ) ventricles ( asin ventricular hypertrophy ). It is not heard in normal individual but can be recorded by phonocardiograph. In abnormal situations like heartfailure,after myocardial infraction etc , the 4thsound is frequently heard

HEART MURMURS :- Murmurs are the adventitious sounds producedwithin the heart, other then the normal heart sounds.These are produced due to turbulence in the blood flow at or near a valve or an abnormal communication within the heart. This turbulence may be created due tovarious reasons like narrowing of a valve or regurgitation through a valve,anaemia etc. Murmurs produced during diastole are called diastolic murmursand those produced during systole are called systolic murmurs.

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