PERSONAL

I have a experience of a rheumatoid arthritis patient who has been admitted in a hospital when the time i actually did know abt her …..She is JXXX(name disclosed) from Chennai . She is a very Gud lady around 35 yrs…..clean mouthed ( less spoken) I love that kind of cases ……..First time i saw her wit her fellow relative that happens to be my fren Mark ( name disclosed ) anyways i was happy she is was fine……….. not till long did i know she was not sufferrin from back pain bcoz of no rest ……and she was suffering from a severe jt pain ….for history sake ill put it here( never miss the history of any patient write it down it almost gives a wide idea on his health status – Dr.KRM)

name : JXXX

age : 35

sex: female

ht : 165cm

wt : 63kgs

bmi: 23.16

occupation : house wife

c/o severe jt pain and more severe towards the back past 4 yrs

progressively increasing for the past month

The patient was absolutely alrite 4 yrs back ….she has history of same symptoms in the past it has been episodically painful and she feels difficult to use her hands on the kitchen and household shores,, she has been a very hardwrkr managing 3 kids and a husband ( she is havin all smaller version devils all 3 and the bigger the naughtier) ………..she later said that she remembers some episode of a fever in the past she has fever and she had severe pain and she was reported she has viral fever and will get ok only by its own…..It took a month n a few more days for her …then she said ……”i felt the same pain the whole month ” …..she was advised to take dolo650mg (paracetomal 650mg she then was alrite then she developed pain again in a 2 months time ………………..she says she has severe pain and cannot move her fingers …………she says she cannot put soap to her back or comb her hair a classical one ( to indian standards) …….wow a GUD case isnt it ????

[({Other details will we entertained on discussions or gmail chat})]

INTRODUCTION

Rheumatoid arthritis (RA) is a form of arthritis that causes pain, swelling, stiffness and loss of function in your joints. It can affect any joint but is common in the wrist and fingers. More women than men get rheumatoid arthritis. It often starts between ages 25 and 55. You might have the disease for only a short time, or symptoms might come and go. The severe form can last a lifetime. Rheumatoid arthritis is different from osteoarthritis, the common arthritis that often comes with older age. RA can affect body parts besides joints, such as your eyes, mouth and lungs. RA is an autoimmune disease, which means the arthritis results from your immune system attacking your body’s own tissues. No one knows what causes rheumatoid arthritis. Genes,viruses, environment and hormones might contribute. Treatments include medicine, lifestyle changes and surgery. These can slow or stop joint damage and reduce pain and swelling.There is NO CURE ….JUST MANAGEMENT IS THE CURRENT TREATMENT ……(REFERENCE EMEDICINE PLUS)

AROUND THE WORLD

The incidence of RA is in the region of 3 cases per 10,000 population per annum. Onset is uncommon under the age of 15 and from then on the incidence rises with age until the age of 80. The prevalence rate is 1%, with women affected three to five times as often as men. It is 4 times more common in smokers than non-smokers. Some Native American groups have higher prevalence rates (5-6%) and people from the Caribbean region have lower prevalence rates. First-degree relatives prevalence rate is 2-3% and diseasegenetic concordance in monozygotic twins is approximately 15-20%. It is strongly associated with the inherited tissue type Major histocompatibility complex (MHC) antigen HLA-DR4 (most specifically DR0401 and 0404) — hence family history is an important risk factor.Rheumatoid arthritis affects women three times more often than men, and it can first develop at any age. The risk of first developing the disease (the disease incidence) appears to be greatest for women between 40 and 50 years of age, and for men somewhat later. RA is a chronic disease, and although rarely, a spontaneous remission may occur, the natural course is almost invariably one of persistent symptoms, waxing and waning in intensity, and a progressive deterioration of joint structures leading to deformations and disability. (Reference wiki)

HOW DO V CALL IT RHEUMATOID ARTHRITIS ??

Jim Mobley, at Pfizer, has discovered a historical pattern of epidemics of tuberculosis followed by a surge in the number of rheumatoid arthritis cases a few generations later. The art of Peter Paul Rubens may possibly depict the effects of rheumatoid arthritis. In his later paintings, his rendered hands show, in the opinion of some physicians, increasing deformity consistent with the symptoms of the disease. The first recognized description of rheumatoid arthritis was in 1800 by the French physician Dr Augustin Jacob Landré-Beauvais (1772–1840) who was based in the famed Salpêtrière Hospital in Paris. The name “rheumatoid arthritis” itself was coined in 1859 by British rheumatologist DrAlfred Baring Garrod.

SO here is the list of the greatest persons wit the disease

1. Dr.Christan Barnard – Heart surgeon

2. Billy Bowden – Criketer

3. Bob Mortimer – British comedian

4. Dr. Dorothy Hodgkin – British chemist Nobel laurette

5. Sandy Koufax – Base ball player

SYMPTOMS AND SIGNS

The symptoms of rheumatoid arthritis come and go, depending on the degree of tissue inflammation. When body tissues are inflamed, the disease is active. When tissue inflammation subsides, the disease is inactive (in remission). Remissions can occur spontaneously or with treatment and can last weeks, months, or years. During remissions, symptoms of the disease disappear, and people generally feel well. When the disease becomes active again (relapse), symptoms return. The return of disease activity and symptoms is called a flare. The course of rheumatoid arthritis varies among affected individuals, and periods of flares and remissions are typical. When the disease is active, symptoms can include fatigue, loss of energy, lack of appetite, low-grade fever, muscle and joint aches, and stiffness. Muscle and joint stiffness are usually most notable in the morning and after periods of inactivity. Arthritis is common during disease flares. Also during flares, joints frequently become red, swollen, painful, and tender. This occurs because the lining tissue of the joint (synovium) becomes inflamed, resulting in the production of excessive joint fluid (synovial fluid). The synovium also thickens with inflammation (synovitis). In rheumatoid arthritis, multiple joints are usually inflamed in a symmetrical pattern (both sides of the body affected). The small joints of both the hands and wrists are often involved. Simple tasks of daily living, such as turning door knobs and opening jars, can become difficult during flares. The small joints of the feet are also commonly involved. Occasionally, only one joint is inflamed. When only one joint is involved, the arthritis can mimic the joint inflammation caused by other forms of arthritis, such as gout or joint infection. Chronic inflammation can cause damage to body tissues, including cartilage and bone. This leads to a loss of cartilage and erosion and weakness of the bones as well as the muscles, resulting in joint deformity, destruction, and loss of function. Rarely, rheumatoid arthritis can even affect the joint that is responsible for the tightening of our vocal cords to change the tone of our voice, the cricoarytenoid joint. When this joint is inflamed, it can cause hoarseness of the voice.

DIAGNOSIS

Several laboratory tests along with a complete physical examination, a health history and X-Rays help in the diagnosis of rheumatoid arthritis. A test called the erythrocyte sedimentation rate (ESR) indicates the presence of any inflammation in the body. In this test a small blood sample is drawn; then the depth that the red blood cells sink to, in a tube in 1 hour is recorded.Another test done with the blood sample helps to determine the presence of rheumatoid factor, an abnormal antibody present in most people who have rheumatoid arthritis. In normal conditions the presence of an antibody is nil. Several laboratory tests along with a complete physical examination, a health history and X-Rays help in the diagnosis of rheumatoid arthritis. A test called the erythrocyte sedimentation rate (ESR) indicates the presence of any inflammation in the body. In this test a small blood sample is drawn; then the depth that the red blood cells sink to, in a tube in 1 hour is recorded.Another test done with the blood sample helps to determine the presence of rheumatoid factor, an abnormal antibody present in most people who have rheumatoid arthritis. In normal conditions the presence of an antibody is nil.

TREATMENT

As such as now there is no complete cure for Rheumatoid arthritis and so there is only management regimens on the basis of the severity . Treatment of rheumatoid arthritis has two components: (1) reducing inflammation and preventing joint damage and disability and (2) relieving symptoms, especially pain. Although achieving the first goal may accomplish the second, many people need separate treatment for symptoms at some point in the disease.

Rheumatoid arthritis is a progressive inflammatory disease. This means that unless the inflammation is stopped or slowed, the condition will continue to get worse in most people. Although rheumatoid arthritis does occasionally go into remission without treatment, this is rare. Starting treatment soon after diagnosis of rheumatoid arthritis is strongly recommended. The best medical care combines medication and nondrug approaches.

Nondrug approaches include the following:

• Physical therapy helps preserve and improve range of motion, increase muscle strength, and reduce pain.
• Hydrotherapy involves exercising or relaxing in warm water. Being in water reduces the weight on your joints. The warmth relaxes your muscles and helps relieve pain.
• Relaxation therapy teaches techniques for releasing muscle tension, which helps relieve pain.
• Both heat and cold treatments can relieve pain and reduce inflammation. Some people’s pain responds better to heat and other’s to cold. Heat can be applied by ultrasound, microwaves, warm wax, or moist compresses. Most of these are done in the medical office, although moist compresses can be applied at home. Cold can be applied with ice packs at home.
• Occupational therapy teaches you ways to use your body efficiently to reduce stress on your joints. It also can help you learn to decrease tension on the joints through the use of specially designed splints. Your occupational therapist can help you develop strategies for coping with daily life by adapting to your environment and using different assistive devices.
• Prosorba column: This is not a drug but a medical device. It filters antibodies linked to rheumatoid arthritis out of the blood. This procedure is available only in some medical centers and generally is used only for very severe rheumatoid arthritis.
• In some cases, reconstructive surgery and/or joint replacement operations provide the best outcome.

• Rheumatoid arthritis was traditionally treated in the past with a stepwise approach starting with nonsteroidal antiinflammatory drugs (NSAIDs) and progressing through more potent drugs such as glucocorticoids, disease-modifying antirheumatic drugs (DMARDs), and biologic response modifiers.
• Over time, however, this strategy was recognized as being faulty, because people treated early with DMARDs have better long-term outcomes, with greater preservation of function, less work disability, and a smaller risk of premature death.
• The goal of drug treatment is to induce remission or at least eliminate evidence of disease activity.
• Early use of DMARDs not only controls inflammation better than less potent drugs but also helps prevent joint damage. Newer DMARDs work better than the older ones in long-term prevention of joint damage.

DMARD’S

Disease-modifying antirheumatic drugs (DMARDs): This group of drugs includes a wide variety of agents that work in many different ways. What they all have in common is that they interfere in the immune processes that promote inflammation in rheumatoid arthritis. DMARDs can actually stop or slow the progression of rheumatoid arthritis. They can also suppress the ability of the immune system to fight infections. Anyone taking one of these drugs must be very vigilant to watch for early signs of infection, such as fever, cough, or sore throat. Early treatment of infections can prevent more serious problems.

• Methotrexate (Rheumatrex, Folex PFS): We do not know exactly how this drug works in the treatment of inflammatory reactions. It relieves symptoms of inflammation such as pain, swelling, and stiffness. People taking methotrexate have to have regular blood tests to measure whether the drug is having any adverse effects on the liver, kidneys, or blood cells. This drug is not suitable for some people with liver problems or women who are or may become pregnant.
• Sulfasalazine (Azulfidine): This drug decreases inflammatory responses by an effect similar to that of aspirin or NSAIDs. People takingsulfasalazine must have regular blood tests to measure whether the drug is having any adverse effects on blood cells.
• Leflunomide (Arava): This drug interferes with cells of the immune system and reduces inflammation. It reduces symptoms and may even slow the progression of rheumatoid arthritis. People taking leflunomide must have regular blood tests to measure whether the drug is having any adverse effects on the liver or blood cells. This agent is not suitable for some people with liver or kidney problems or women who are or may become pregnant.
• Gold salts (aurothiomalate, auranofin [Ridaura]): These compounds contain very tiny amounts of the metal gold. We do not know why they stop inflammation. Apparently, the gold infiltrates into immune cells and interferes with their activities. People taking gold must have regular blood and urine tests to measure whether the drug is having any adverse effects on blood cells and the kidney.
• D-penicillamine: This agent combines with metals in the bloodstream and cells and removes them from the body. This suppresses certain actions of the immune system that promote rheumatoid arthritis. People taking D-penicillamine must have regular blood and urine tests to measure whether the drug is having any adverse effects on blood cells and the kidney.
• Hydroxychloroquine (Plaquenil): This drug was first used against the tropical parasite malaria. It inhibits certain cells that are necessary for theimmune response that causes rheumatoid arthritis. People takinghydroxychloroquine must have eye examinations at least yearly to determine whether the drug is having any adverse effects on the retina.
• Azathioprine (Imuran): This drug stops the production of cells that are part of the immune response associated with rheumatoid arthritis. Unfortunately, it also stops production of some other types of cells and thus can have serious side effects. It strongly suppresses the entire immune system and thus leaves the person vulnerable to infections and other problems. It is used only in severe cases of rheumatoid arthritis that have not gotten better with other DMARDs. People taking azathioprinemust have regular blood tests to measure wither the drug is having any adverse effects on blood cells. It is not used for women who are or may become pregnant.
• Cyclosporine (Neoral): This drug was developed for use in people undergoing organ transplantation or bone marrow transplantation. These people must have their immune system suppressed to preventrejection of the transplant. Cyclosporine blocks an important immune cell and interferes with the immune response in several other ways. People taking cyclosporine must have regular blood tests and blood pressurechecks to measure whether the drug is having any adverse effects on blood cells and blood pressure. It is not used for women who are or may become pregnant.

Biologic response modifiers: These agents act like substances produced normally in the body and block other natural substances that are part of the immune response. They block the process that leads to inflammation and damage of the joints.

• Etanercept (Enbrel): This agent blocks the action of tumor necrosisfactor, which in turn decreases inflammatory and immune responses. It is given by subcutaneous injection twice weekly. People taking etanerceptmust have regular blood tests to measure whether the drug is having any adverse effects on blood cells.
• Infliximab (Remicade): This antibody blocks the action of tumor necrosis factor. It is often used in combination with methotrexate in people whose rheumatoid arthritis does not respond to methotrexate alone. It is given by intravenous infusion every six to eight weeks. People takinginfliximab must have regular blood tests to measure whether the drug is having any adverse effects on blood cells.
• Adalimumab (Humira): This is another blocker of tumor necrosis factor. It reduces inflammation and slows or stops worsening of joint damage in fairly severe rheumatoid arthritis. It is given by subcutaneous injection every two weeks. People taking adalimumab must have regular blood tests to measure whether the drug is having any adverse effects on blood cells.
• Anakinra (Kineret): This agent blocks the action of interleukin-1, which is partly responsible for the inflammation of rheumatoid arthritis. This in turn blocks inflammation and pain in rheumatoid arthritis. This agent is usually reserved for people whose rheumatoid arthritis has not improved with DMARDs. It is given by subcutaneous injection daily. People takinganakinra must have regular blood tests to measure whether the drug is having any adverse effects on blood cells.

SURGICAL METHODS

Some people with rheumatoid arthritis need several operations over time. Examples include removal of damaged synovium (synovectomy), tendon repairs, and replacement of badly damaged joints, especially the knees or hips. Some people with rheumatoid arthritis have involvement of the vertebrae of the neck (cervical spine). This has the potential for compressing the spinal cord and causing serious consequences in the nervous system. These people occasionally need to undergo surgical fusion of the spine.

REGULAR VISIT

Regardless of whether a specialist or your primary-care provider is treating you for rheumatoid arthritis, he or she should see you regularly to monitor your condition, your response to treatment, and side effects and other problems related to your rheumatoid arthritis or your treatment. The best way to monitor your condition is to see if you have any disability (loss of function) and, if so, how much. The frequency of these visits depends on the activity of your rheumatoid arthritis. If your treatment is working well and your condition is stable, the visits can be less frequent than if your rheumatoid arthritis is getting worse, you are developing complications, or you are having severe side effects of treatment. Each person’s situation must be decided individually

Hehhehehehehe This Bcoz of a Personal Experience in cramps..There are a lot a people sufferring from this everyday problem……and today me too ..There was days that this muscle cramps have almost killed me ..I have a sweet belly and im not that old …Im lazy …I dont do my warm ups ….I straight away go for the exercise …..I do the Abs in first place….Then i have a very bad cramp…..this is not new to me …I have been doing this for like some 10 yrs from now …and im still doin this………. Today i just wanted to know how is this cramp happening …..Just checked out …whats the phenomena ???? whats the physiology ?????why is it happening  ????

What is a Cramp?????

Cramps are unpleasant, often painful sensations caused by contraction or over shortening of muscles. Cramps can be caused by cold, overexertion, or a low calcium level in the blood (especially for adolescents, who need calcium for both blood and bone maturation). …

How Does it Occur???

Cramps can occur in two types :-

1) EXERCISE INDUCED]

Exercising is probably the most common cause of muscle cramps. Exercising hard cause small rips in the muscles. When the muscles are being worked too hard, they can respond by cramping up. Cramps are also caused by hyperflexion–bending a joint beyond where it is supposed to bend. This can cause the muscles to contract protectively, resulting in pain and stiffness. Dehydration and lactic acid buildup also contribute to exercise-induced muscle cramps. Basically, anything that works your body really hard can cause cramps.

2) OTHER CAUSES

Lack of oxygen can cause muscles to cramp up. People with poor circulation due to arteriosclerosis often get muscle cramps in their legs–especially when exercising. Low levels of certain minerals, such as salt or calcium, can also lead to muscle cramps. Rapid changes in temperature can also lead to muscle cramping–especially when the temperature cools quickly. Finally, muscle cramps can be caused by some serious illnesses, such as thyroid disease, kidney disease and multiple sclerosis.

Whats happening ???

Muscle cramps can be caused by nerves that malfunction. Sometimes this malfunction is due to a health problem, such as a spinal cord injury or a pinched nerve in the neck or back. Other causes are

• Straining or overusing a muscle
• Dehydration
• A lack of minerals in your diet or the depletion of minerals in your body
• Not enough blood getting to your muscles

For Abs cramp???

I commonly do abs bcoz i have a big tummy and im not into regular exercises too bcoz of my useless shedule and my laziness to work out ……..But still everytime i do ABS i have CRAMPS…………………and i really suffer ….Cry …..Shout …. Call for Help ……. and last releive my self lying in the same place……..Shud we do this……………NO ……but follow this ………………If you are doing abdominal exercises in the hopes of getting a strong core and a flat stomach, you aren’t alone. Ab exercises are some of the most popular exercises for both novice and elite athletes. However to get a flat belly and defined abs takes more than just crunches. You also need to reduce the layer of body fat covering up your well-defined abs………..There are many exercises you can do to work the abs. There are also some great products that you can use at home, such as a large exercise ball. Using the ball for crunches requires that you stabilize your torso while balanced on the ball and you end up using more muscles than when performing standard crunches…………

Diet during exercises????

In order to decrease body fat and gain muscle requires proper nutrition. You’ll need a balanced diet of carbohydrate, protein and fat. Eating several small meals throughout the day helps many people stay more satisfied and reduces hunger. Other tips for avoiding fat gain include: getting calcium, eating breakfast and eating high fiber foods. Make sure you stay well-hydrated by drinking water throughout the day and be sure not to cut calories too drastically or you could inadvertently lower your metabolism…..

Ynot aerobics???

Aerobic exercise is the best way to burn calories and manage (or lose) weight. Reducing your calories without exercise will lead to initial weight loss, but you’ll likely reach a plateau and you may also lose muscle. A personal exercise plan will get you past plateaus and can help you maintain muscle…..

THEN WAT????

It was the biggest of all times when we human world just discovered syphilis as a great sexual disease,  and was one of the most competitive issues in medical treatment of the 1900’s and even bfore it was found………Why is it we have syphilis through sexual encounters ???? wats its history ??how can i find it ?? Where can we get it more commonly??? the risk factors ?? how does the signs look like ??? wat are the comon symptoms ????? Is it a better managed disease ??? how easier its treatable ………..this is not the commonly asked qns …this is the first some few qns i had when i was in the 1st year itself …It has always been a trouble to all teenagers about the sexually transmitted diseases…..is it ???????? I think so !!!!!!!!!!

HISTORY OF SYPHILIS ??

Three theories on the origin of syphilis have been proposed. It is generally agreed upon by historians and anthropologists that syphilis was present among the indigenous peoples of the Americas before Europeans traveled to and from the New World. However, whether strains of syphilis were present in the entire world for millennia, or if the disease was confined to the Americas in the pre-Columbian era, is debated.

1. PRECOLUMBIAN THEORY
2. COLUMBIAN THEORY- During Columbus times
3. COMBINATION THEORY -Alfred Cosby

FIRST MEDICINE

The Spanish priest Francisco Delicado wrote El modo de adoperare el legno de India (Rome, 1525) about the use of Guaiacum in the treatment of syphilis. He himself suffered from syphilis.

SECOND MEDICINE

Then it was of no use so they had to use mercury which was a dreadful drug again. Nicholas Culpeper recommended the use of heartsease (wild pansy), an herb with antimicrobial activities. Another common remedy was mercury: the use of which gave rise to the saying “A night in the arms of Venus leads to a lifetime on Mercury“.It was administered multiple ways including by mouth, by rubbing it on the skin and by injection. One of the more curious methods was fumigation, in which the patient was placed in a closed box with his head sticking out. Mercury was placed in the box and a fire was started under the box that caused the mercury to vaporize. It was a grueling process for the patient and the least effective for delivering mercury to the body. The use of mercury was the earliest known suggested treatment for syphilis. But was defintly better than guaiacum .

THIRD MEDICINE

The first antibiotic to be used for treating disease was the arsenic-containing drug Salvarsan, developed in 1908 by Sahachiro Hata while working in the laboratory of Nobel prize winner Paul Ehrlich.This was later modified into Neosalvarsan. Unfortunately, these drugs were not 100% effective, especially in late disease. It had been observed that some who develop high fevers could be cured of syphilis. Thus, for a brief time malaria was used as treatment for tertiary syphilis because it produced prolonged and high fevers (a form of pyrotherapy).

ROLE OF QUININE’S

This discovery was championed by Julius Wagner-Jauregg, who won the 1927 Nobel Prize for Medicine for his work in this area. Malaria as a treatment for syphilis was usually reserved for late disease, especially neurosyphilis, and then followed by either Salvarsan or Neosalvarsan as adjuvant therapy.

PENICILLIN MADE ENTRY

hese treatments were finally rendered obsolete by the discovery of penicillin, and its widespread manufacture after World War II allowed syphilis to be effectively and reliably cured

GOT BORED

This is not it there are great persons in the past and less  persons in the future going to be a victim of syphilis . There is a very big list of the persons and u will be amazed by the people bcoz most of them are who we know

1. Charles VIII France
2. Hernando Cortez
3. Adolf Hitler
4. Benito Mussolini
5. Vladimir Ilyich Lenin
6. Leo Tolstoy
7. Maurice Barrymore
8. Henry VIII
9. Ivan the Terrible
10. Martin Alonso Pinzon
11. Eleanor of Toledo
12. Hugo Wolf
13. Lord Randolph Churchill
14. Vincent van Gogh
15. Jack Pickford

and there are wat more of famous citizens in the world who were victims of this disease and this is just a list that i know and there are more n more u may be knowing .

WAT ARE THE SIGNS & SYMPTOMS OF SYPHILIS???

The symptoms of syphilis are the same in men and women. They can be mild and difficult to recognise or distinguish from other STDs. Symptoms may take up to 3 months to appear after initial infection. Syphilis is a slowly progressing disease that has several stages. The primary and secondary stages are very infectious.

There are 3 stages of Syphilis :-

1. Primary syphilis

2. Secondary Syphilis

3. Tertiary Syphilis

an the symptoms differs for all

PRIMARY SYPHILIS

• -21 Days approximately from the time of sexual contact with the infected person

• -one or more painless ulcers called as chancres

• -highly infectious
• -chancres on vagina(f), cervix(f), Penis(m), Mouth, and around anus(both)
• -without treatment they take around 2-6 wks to heal
• - If it does not heal it progresses to  secondary syphilis

SECONDARY SYPHILIS

• -Primary syphilis which is not subsiding within next 3-6 wks causes secondary syphilis
• -flu like illness
• -loss of appetite
• -swollen glands (wks to months )
• -non itchy rash or patches all over the body
• -warty growths in vulva(f)  and anus(both)
• -white patches on tongue and mouth
• -Alopecia
• -The most infective stage of syphilis and sexual transmission clearly trasmits syphilis
• -this may settle in a few weeks or months but may be latent for months to years in the induividual and can actively spread
• -treatment at this stage can cause a sure cure for syphilis but dont wait for this or else in the 3rd stage you are going to go MAD

TERTIARY SYPHILIS / NEUROSYPHILIS

• If a person infected with syphilis has not received treatment during the first two stages of the disease then it will progress to the latent stage.
• The person will no longer experience any symptoms of the earlier stages, but their infection can still be diagnosed with a blood test.
• If left untreated, the infection may develop into symptomatic late syphilis, also known as the tertiary stage.
• This usually develops after more than 10 years and is often very serious. It is at this stage that syphilis can affect the heart and possibly the nervous system.
• If treatment for syphilis is given during the latent stage the infection can be cured.
• However, any heart or nervous-system damage that occurred before the start of treatment may be irreversible.

WAT IS THE ORGANISM CAUSING ???

Mainly Syphilis is caused by Treponema Palladium. Treponema pallidum is a species of spirochaete bacterium with subspecies that cause treponemal diseases such as syphilis, bejel, pinta and yaws. It is not seen on a Gram stained smear because the organism is too thin.

Subspecies

There are at least four known subspecies:

• Treponema pallidum pallidum, which causes syphilis
• T. pallidum endemicum, which causes bejel
• T. pallidum carateum, which causes pinta
• T. pallidum pertenue, which causes yaws

There is some variation as to which are considered subspecies, and which are species. The cause of pinta is sometimes described as “Treponema carateum”, rather than a subspecies of Treponema pallidum, even when the subspecies convention is used for the other agents.

DIAGNOSIS ???

DARK FIELD MICROSCOPY

Dark-field microscopy is the most specific technique for diagnosing syphilis when an active chancre or condyloma latum is present. However, its accuracy is limited by the experience of the operator performing the test, the number of live treponemes in the lesion, and the presence of non-pathologic treponemes in oral or anal lesions. In preparation for dark-field microscopy, the lesion is cleansed and then abraded gently with a gauze pad. Once a serous exudate appears, it is collected on a glass slide and examined under a microscope equipped with a dark-field condenser. Negative examinations on three different days are necessary before a lesion may be considered negative for T. pallidum

OTHERS TESTS

1. VDRL
2. Rapid Plasma Reagin Test

False positive seen in many no: of cases with Pregnancy, Autoimmune diseases and Infections

SPECIFIC TEST

These tests are used primarily to confirm the diagnosis of syphilis in patients with a reactive nontreponemal test. However, the enzyme immunoassay (EIA) test for antitreponemal IgG also may be used for screening. Treponemal-specific tests include the

1. EIA for anti-treponemal IgG,
2. the T. pallidum hemagglutination (TPHA) test,
3. the microhemagglutination test with T. pallidum antigen,
4. the fluorescent treponemal antibody-absorption test (FTA-abs),
5. and the enzyme-linked immunosorbent assay.

TREATMENT ???

PRIMARY SYPHILIS

Primary syphilis is treated with 2.4 million units of penicillin G benzathine delivered intramuscularly in a single dose. In nonpregnant patients who are allergic to penicillin, alternative regimens include doxycycline (Doxy1), in a dosage of 100 mg taken orally twice daily for two weeks, or tetracycline, in a dosage of 500 mg taken orally four times daily for two weeks. Limited evidence indicates that Ceftriaxone , in a dosage of 1 g delivered intramuscularly or intravenously once daily for eight to 10 days, or azithromycin (Azibact), in a single 2-g dose taken orally, may be effective for the treatment of primary syphilis.

SECONDARY SYPHILIS

Treatment employs the same antibiotic regimens used for primary syphilis. Follow-up is the same as that for primary syphilis.

TERTIARY SYPHILIS

Antibiotic therapy for gummatous and cardiovascular syphilis is the same as that for late latent syphilis, provided no evidence of neurologic involvement is present. Consensus is lacking on the appropriate follow-up in patients who have tertiary syphilis with no CNS involvement. Clinical response to treatment varies and depends on the type and location of gummatous or cardiovascular lesions.

TABES DORSALIS ????

Tabes dorsalis (locomotor ataxia) involves slow, progressive degeneration of the posterior columns and nerve roots. It typically develops 20 to 30 yr after initial infection; mechanism is unknown. Usually, the earliest, most characteristic symptom is an intense, stabbing (lightning) pain in the back and legs that recurs irregularly. Gait ataxia, hyperesthesia, and paresthesia may produce a sensation of walking on foam rubber. Loss of bladder sensation leads to urine retention, incontinence, and recurrent infections. Erectile dysfunction is common. Most patients with tabes dorsalis are thin and have characteristic sad facies and Argyll Robertson pupils (pupils that accommodate for near vision but do not respond to light). Optic atrophy may occur. Examination of the legs detects hypotonia, hyporeflexia, impaired vibratory and joint position sense, ataxia in the heel-shin test, absence of deep pain sensation, and Romberg’s sign. Tabes dorsalis tends to be intractable even with treatment. Visceral crises (episodic pain) are a variant of tabes dorsalis; paroxysms of pain occur in various organs, most commonly in the stomach (causing vomiting) but also in the rectum, bladder, and larynx.

PARENCHYMATOUS NEUROSYPHILIS???

It usually develops 15 to 20 yr after initial infection and typically does not affect patients before their 40s or 50s. Behavior progressively deteriorates, sometimes mimicking a mental disorder or dementia. Irritability, difficulty concentrating, deterioration of memory, defective judgment, headaches, insomnia, fatigue, and lethargy are common; seizures, aphasia, and transient hemiparesis are possible. Hygiene and grooming deteriorate. Patients may become emotionally unstable and depressed and have delusions of grandeur with lack of insight; wasting may occur. Tremors of the mouth, tongue, outstretched hands, and whole body may occur; other signs include pupillary abnormalities, dysarthria, hyperreflexia, and, in some patients, extensor plantar responses. Handwriting is usually shaky and illegible.

MENINGOVASCULAR NEUROSYPHILIS??

Inflammation of large- to medium-sized arteries of the brain or spinal cord; symptoms typically occur 5 to 10 yr after infection and range from none to strokes. Initial symptoms may include headache, neck stiffness, dizziness, behavioral abnormalities, poor concentration, memory loss, lassitude, insomnia, and blurred vision. Spinal cord involvement may cause weakness and wasting of shoulder-girdle and arm muscles, slowly progressive leg weakness with urinary or fecal incontinence or both, and, rarely, sudden paralysis of the legs due to thrombosis of spinal arteries.

JARISCH-HERXHEIMER REACTION??

Most patients with primary or secondary syphilis, especially those with secondary syphilis, have a JHR within 6 to 12 h of initial treatment. It typically manifests as malaise, fever, headache, sweating, rigors, anxiety, or a temporary exacerbation of the syphilitic lesions. The mechanism is not understood, and JHR may be misdiagnosed as an allergic reaction. JHR usually subsides within 24 h and poses no danger. However, patients with general paresis or a high CSF cell count may have a more serious reaction, including seizures or strokes, and should be warned and observed accordingly. Unanticipated JHR may occur if patients with undiagnosed syphilis are given antitreponemal antibiotics for other infections.

CONDYLOMO LATA ??

hypertrophic, flattened, dull pink or gray papules at mucocutaneous junctions and in moist areas of the skin (eg, in the perianal area, under the breasts); lesions are extremely infectious. Lesions of the mouth, throat, larynx, penis, vulva, or rectum are usually circular, raised, and often gray to white with a red border. Secondary syphilis can affect any organ. About ½ of patients have lymphadenopathy, usually generalized, with nontender, firm, discrete nodes, and often hepatosplenomegaly. About 10% of patients have lesions of the eyes (uveitis), bones (periostitis), joints, meninges, kidneys (glomerulitis), liver (hepatitis), or spleen. About 10 to 30% of patients have mild meningitis, but < 1% have meningeal symptoms, which can include headache, neck stiffness, cranial nerve lesions, deafness, and eye inflammation (eg, optic neuritis, retinitis).

CONGENITAL SYPHILIS

present in utero and at birth, and occurs when a child is born to a mother with secondary syphilis. Untreated syphilis results in a high risk of a bad outcome of pregnancy, including Mulberry molars in the fetus. Syphilis can cause miscarriages, premature births, stillbirths, or death of newborn babies. Some infants with congenital syphilis have symptoms at birth, but most develop symptoms later. Untreated babies can have deformities, delays in development, or seizures along with many other problems such as rash, fever, swollen liver and spleen, anemia, and jaundice. Sores on infected babies are infectious.

PREVENTION??

Methods of prevention of Syphilis mentioned in various sources includes those listed below. This prevention information is gathered from various sources, and may be inaccurate or incomplete. None of these methods guarantee prevention of Syphilis.

• Safe sex
• Monogamy
• Condoms
• Pregnancy screening for syphilis – avoids congenital syphilis in the newborn.

INTRO

Hehehehehehehe ……………..The one thing which has made a substitute for INSULIN…………….the only drug of choice for a early diagnosed and well diet controlled patient with Non insulin diabetes mellitus  ……….

Oral hypoglycemic agents commonly are referred to as sulfonylureas, a class of compounds. Sulfonylurea compounds are among the most widely prescribed medications in the world. The drugs are frequently used to treat patients with type II diabetes. Wide availability of these medications increases potential for either intentional or unintentional overdose in pediatric and adult populations.

First-generation sulfonylurea compounds became widely available in 1955. They are acetohexamide, chlorpropamide, tolazamide, and tolbutamide. First-generation agents have longer half-lives (eg, 49 hours for chlorpropamide). Second-generation sulfonylureas were introduced in 1984. Known as glipizide, glyburide, and glimepiride, second-generation sulfonylureas are more potent and have shorter half-lives than the first-generation sulfonylureas.

Other agents besides sulfonylureas are used to treat type II diabetes, including biguanides, alpha-glucosidase inhibitors, and troglitazone. Metformin (Glucophage in the United States) is one such agent. Even in excessive dosage, these agents do not decrease serum glucose below euglycemia; consequently, they are referred to appropriately as antihyperglycemic agents rather than hypoglycemic agents.

The Joslin Diabetes Center released a clinical guideline for the pharmacological management of type II diabetes in 2007.

CLASSIFICATION OF DRUGS

1. SULFONYL UREA’S
2. BIGUANIDES
3. ALPHA GLUCOSIDASE INHIBHITORS
4. MEGLITINIDES
5. THIAZOLINEDIONES

SULFONYLUREA’S

Sulfonylureas work primarily by stimulating pancreatic insulin secretion, which in turn reduces hepatic glucose output and increases peripheral glucose disposal.

preparation of sulfonylurea

The sulfonylureas are often classified as belonging to the first or second generation.

The First generation sulfonylureas:

• Acetohexamide
• Chlorpropamide
• Tolazamide
• Tolbutamide.

The Second generation sulfonylureas :

• Glibenclamide
• Glyburide
• Glipizide
• Glicazide
• Glimepiride

The first generation sulfonylureas are rarely used now.

NEWER DRUGS ARE Glimipiride (Amaryl) and Glicazide MR and XR ………Nowadays new medicine is used vastly in the practice of longterm NIDDM cases (Non insulin dependant Diabetes Mellitus)……..

Also available in 60 mg and even in XR(xtended release)

The SU class of oral hypoglycemic agents (insulin secretagogues) has been in existence since tolbutamide was introduced in 1956.

The sulfonylurea drugs have effects which are still not completely understood. Initially, they work primarily by stimulating pancreatic insulin secretion, which in turn reduces hepatic glucose output and increases peripheral glucose disposal. They are potassium channel blockers whose effect on the pancreatic beta-islet cells is to allow an influx of calcium into the cell, which causes an increase in the release of insulin.

depletion of Beta cells

However, after several months, blood levels of insulin return to pre-medication levels, yet blood glucose levels remain reduced. Clearly, the sulfonylurea drugs must have other effects. Several have been identified, among them: sulfonylurea medications slow the rate at which the liver releases glucose into the bloodstream, and they increase the number of insulin receptors on cell membranes, thus increasing insulin efficiency.

The efficacy of the first- and second-generation sulfonylureas is similar, although second-generation agents are better formulated and, although costlier than the older sulfonylureas, have some advantages. Second-generation sulfonylureas:

Are more potent on a per milligram basis
Tend to produce fewer side effects
In addition, the pharmacokinetics of these second-generation agents allows for more effective once-a-day dosing, which enhances compliance.

Although some consider SUs to be dated compared with the newer oral hypoglycemic drugs, there remains a large number of patients that will continue to benefit from them.

BIGUANIDES

Two drugs in this category are phenformin and metformin.

Metformin_500mg_Tablets

Biguanides work mainly by

• Suppressing excessive hepatic glucose production
• Increasing glucose utilization in peripheral tissues to a lesser degree.
• Possibly reduce food intake and thus reduce intestinal glucose absorption

Metformin structure

As the biguanides do not stimulate endogenous insulin secretion, hypoglycemia does not occur when they are used alone and therefore they are sometimes called anti-hyperglycemic agents rather hypoglycemic agents.

The use of phenformin has decreased considerably and it is usually metformin that is now used when a biguanide is prescribed.

The biguanides were introduced in 1957. Both phenformin and metformin have been widely used here, although in recent times, the use of phenformin has decreased significantly and most people now use metformin when a biguanide is to be used.

Metformin works mainly by suppressing excessive hepatic glucose production, although it may increase glucose utilization in peripheral tissues to a lesser degree, by decreasing insulin resistance in muscle cells. Metformin may also improve glucose levels by reducing intestinal glucose absorption.

Metformin is not metabolized and is excreted unchanged by the kidneys.

Metformin effects

Metformin has many characteristics that are ideal for treating type 2 diabetes, including weight loss, insulin sensitization, positive lipid effect, mild hypotensive effect, and low or no incidence of hypoglycemia.

Because metformin does not stimulate endogenous insulin secretion, hypoglycemia does not occur when this dose is used alone, although hypoglycemia may occur if metformin is taken with insulin, a sulfonylurea, or an excessive amount of alcohol.

Treatment with metformin has beneficial effects on plasma lipids (it lowers triglyceride and low-density lipoprotein [LDL] cholesterol levels while increasing high-density lipoprotein [HDL] cholesterol) that are greater than expected from improved glucose control alone.

In addition, metformin therapy has been associated with weight loss or no weight gain. This may be particularly helpful in obese patients with type II diabetes.

Metformin is effective as monotherapy or in combination with sulfonylureas, alpha-glucosidase inhibitors, and insulin. The combination of metformin and troglitazone has also been shown to be safe and effective, although this combination is not an USA FDA- approved indication and extensive published data on this combination is lacking.

ALFA GLUCOSIDASE INHIBHITORS

miglitol structure

There are Acarbose and Miglitol. Acarbose (Precose) is an alpha-glucosidase inhibitor that slows down the breakdown of disaccharides and polysaccharides and other complex carbohydrates into monosaccharides. The enzymatic generation and subsequent absorption of glucose is delayed and the postprandial blood glucose values, which are characteristically high in patients with type II diabetes, are reduced with acarbose. AGIs do not prevent the absorption of carbohydrates and complex sugars, but they do delay their absorption.

Acarbose structure

Delaying the absorption of carbohydrates is a unique mechanism among oral diabetic medications for lowering HgbA1c levels. The effectiveness of this mechanism is one of the physiologic characteristics of type 2 diabetes. Patients with type 2 diabetes demonstrate a delayed or sluggish insulin response from the pancreas to a glucose (a meal) load. By delaying the absorption of glucose, the insulin response is more matched to the serum glucose, resulting in less postprandial hyperglycemia and a lowering of the HbA1c. The AGIs also demonstrate a lowering of total insulin output of the pancreas, increased insulin sensitivity, a variable but mild decrease in triglycerides, with no effect on patient weight.

One disadvantage with the use of acarbose is that it is to be taken along with the first bite of a meal. Moreover, it has to be taken three times daily with meals. These factors often lead to non compliance and a decrease in the efficacy of the drug.

MEGLITINIDES +AMINOACID DERIVATIVES

A very recent addition to the OHA group. It is a ultra short acting drug which acts directly on the the beta cells of the pancreas and increases the secretion of insulin. It also corrects the problems with the pulsatile release of insulin which is seen in Type II diabetes.

Repaglinide from the meglitinide drug class, acts like an extremely short-acting SU (an insulin secretagogue) and is potentially useful as a SU replacement. The effect of repaglinide on the pancreas is very similar to that of the SUs. Repaglinide, like the SUs, blocks the potassium channels on the pancreatic islet beta-cells, which causes an influx of calcium into the cell and increasing the secretion of insulin. There appears to be 2 similar potassium channels on islet beta-cells, one of which is predominantly affected by repaglinide and the other is predominantly affected by SUs.

Repaglinide structure

The repaglinide-affected potassium channel appears to be glucose dependent, which may partially explain why repaglinide is associated with a much lower incidence of hypoglycemia.

novonorm- repaglinide

What makes repaglinide clinically different from the SUs is its ultra-short half-life (1 hour). Repaglinide is taken just before or with meals, and the stimulation of the pancreas is limited only to a brief time around meals. Because of the short duration, the patient does not have continuous high levels of insulin and the resulting adverse effects.

Its biggest advantage over the other oral hypoglycemic medications is that it allows for flexible timing and missed meals.

Repaglinide has been approved for use with metformin, and the combination appears to be a very effective. There are no clinical trials of repaglinide with the alpha-glucosidase inhibitors, and of the TZD class, only 1 clinical trial with troglitazone has been reported. There are theoretical interactions between repaglinide and the TZDs through their common metabolism in the P450 pathway, so more clinical trials are clearly needed.

THIAZOLIDINEDIONES

Rosiglitazone structure

Thiazolidinediones are a new class of oral antidiabetic agents (commercially known as glitazones) that enhance insulin sensitivity in peripheral tissues. Troglitazone was the first glitazone introduced to the market, and though widely used, it has now been withdrawn from the market as its use has been linked with hepatocellular injury and death secondary to liver failure.

Rosiglitazone and Pioglitazone are now available for clinical use and are extremely potent in reducing peripheral insulin resistance.

The thiazolidinedione (TZD) class of oral hypoglycemics ( popularly known as glitazones) was developed in 1997 and offers a new mechanism for treatment of type 2 diabetes. The first, troglitazone was taken off the market in 1999 because of its association with hepatic toxicity. Rosiglitazone and pioglitazone have been available since 1999, and have recently been introduced in the Indian market.

The primary effect of TZDs is peripheral, with increasing insulin sensitivity and increased glucose uptake. The TZDs have some effect on hepatic glucose uptake and sensitivity to a lesser degree. They do not stimulate the pancreas to produce more insulin.

TZDs are hepatically metabolized and thus can be used safely in patients with renal dysfunction. They can be dosed once daily, although rosiglitazone works better with twice-daily dosing. Reports have suggested that rosiglitazone works better in women, but the reason for this is not known.

Both pioglitazone and rosiglitazone are approved for monotherapy and in combination with metformin, SUs, and insulin.

Besides their effect in lowering the blood glucose levels, both drugs also have notable effects on lipids. The current data show that pioglitazone has a minimal effect on low-density lipoprotein (LDL) cholesterol levels and a favorable effect on high-density lipoprotein (HDL) cholesterol and triglyceride levels. Rosiglitazone has a favorable effect on HDL cholesterol levels but a negative effect on LDL cholesterol levels.

With use of glitazones, patience is required. Blood sugar levels may show a significant reduction statistically in as little as two to four weeks, but the maximum effects are not seen until two or three months have passed.

CONCLUSION

So i dont have a conclusin yet……………………Postin it soon !!!!!!!!!!!!!!!!!!!!!!!!

INTRODUCTION

Sri krishna Hospital is at New Military Road, Avadi, Chennai -600062 . Dr.C.Jayapal BSc MD (CARDIOLOGY) has also recieved a lot a rewards from the Institute of Diabetology and has been very very sucessful in his diabetic practice and has been receiving a lot of good outcome from most of his patients …………………I was shell shocked the first day i joined there …that was 02/01/2010 ….a day that gave my life  a big big change ……..

ABT THE PRACTICE THERE

All patients there are interesting xcept for a few malingering cases ……………..the first case of my life was a TB patient at BH(Bombay hospital) a very well pronouned Hospital in the world ……………..but a lot of cases die out of poor patient care by the staff nurses ……bcoz the docs are trained better there and the nurses are not upto the mark…………………His name was Trilok /45/m from wadala(mumbai)…………..he was a businessman and suffered from TB ….Non smoker / Non drinker and also  a Vegeterian……….But he only survived of a very innate care take by Dr.K.Ramamoorthy MD the messiah of the Hospital………But here the story stands all behind the sucess of a single hero who has made his life so long in the history of medicine and who has dedicated himself to medicine ……………………..He is Dr.C.Jayapal MD from Krishna Hospital …..“Its like everyday learning hahahha ” the same words ……I just stole it from his mouth ….Looks nice to hear ….but more nicer  to xperience ………he always makes  a proper History taking and Xamines every single patient from hair to toe nail …….and also follows the course of the disease and treats according to the disease and not according to the symptom…….Bcoz it may cost him a lot of workin hours ……He is also a great devotee of Lord krishna and a life member of the ISKON trust ….and also has his own temple abt a 2 km   from Avadi. …..So he has a very good power on Speech and thought and learn like no 2 moro…..and teaches like the god krishna himself ,,,,,,,But the class he follows is very very simple …….he is like a 2nd yr MBBS student xaminig each case thoroughly very rarely missin any …….but his staffs are also not upto mark ……so his maintanence of inpatients has been not that sucessful compared to his blaring practice ….there are patients from even differents states and districts …….But his teaching has been a very good mark on my medical life ….Im very happy to inform u that he is my Chacha (chitappa, Kochuacchan, Fathers yunger brother )……

NEW IDEAS IN ME

This wondrful xperience of my life shud be shared by my frens and fellow viewers and also my dear readers and my patients and his patients too ….so plannin to write Blogs on Diabetes Mellitus ………………………………. and have to make a safe world and better country …………………………we are leading in oral cancers in the world 80% and next in DM 40 % and mostly in the developed states of the country ……….So there shud be proper education for the pople and the doctors to be well developed in their methods of proper learning abt the disease and the symptom…………………..understand its not the symptom creating the problem its the disease …………………same  way there is no proper treatment without necessary investigations and there is no proper treatment without management of the disease itself …………………………….

Regards

urs always DR.LOKKU (LOGARANGAN MUTHURANGAN)

Y suffer when u know the Better

What is gonorrhea ?????

A sexually transmitted Disease (STD) caused by the bacterium Neisseria gonorrhoea. Although gonorrhea is known primarily as a sexually transmitted Disease (STD), it is not exclusively so, but can also be transmitted to the newborn during the birthing process.

What was it called Before ????

Gonorrhea is sometimes also known as “the clap”. This moniker may seem a bit strange but is has actually been around since 1587. It comes from the French word “clapoir” which was commonly used to describe gonorrhea in the late sixteenth century.

How is it spread????

Contrary to popular belief, gonorrhea cannot be transmitted from toilet seats or door handles. The bacterium Neisseria gonorrhea requires very specific conditions to grow and to reproduce. It cannot live outside the body for more than a few minutes at most, nor can it live on the skin of the hands, arms, or legs. It survives only on moist surfaces within the body and is found most commonly in the vagina and, especially the cervix. The bacterium can also live in the urethra. Gonorrhea can even exist in the back of the throat (from oral-genital contact) and in the rectum.

Gonorrhea is not a small problem ????

Left untreated, gonorrhea can lead to a severe painful pelvic infection with inflammation of the fallopian tubes and ovaries, a form of pelvic inflammatory disease, or PID. Symptoms of PID include fever, pelvic cramping, abdominal pain, and pain with intercourse. PID can lead to difficulty in becoming pregnant or even sterility.

Can Gonorrhea Complicate ????

The complications of gonorrhea can include inflammation of the heart valves, arthritis, and eye infections. If the infection is severe enough, a localized area of infection and pus (an abscess) forms, and major surgery may be necessary and even life-saving. Gonorrheal infection in people with diminished immune function, such as from chemotherapy or AIDS, can also be extremely serious.

Gonorrhea can also cause eye Infections !!!!!

Gonorrhea can cause eye infections in babies born to infected mothers, even if the mother has no symptoms at the time of delivery. Chlamydia can also be passed from mother to child during birth. Infected newborn infants develop drainage from the eyes within 2 weeks of birth and the eyelids become puffy, red, and tender. Gonorrhea may cause perforation of the cornea and very significant destruction of the deeper eye structures while chlamydia is somewhat less destructive. Hospitals require silver nitrate or, more often today, antibiotic drops in a newborn’s eyes to prevent these diseases.

Symptoms of Gonorrhea ???

The early symptoms of gonorrhea often are mild, and some people who are infected have no symptoms of the disease; this is one reason why it is so readily transmitted. If symptoms of gonorrhea develop, they usually appear within 2 to 10 days of sexual contact with an infected partner, although a small percentage of patients may be infected for several months without showing symptoms.

The initial symptoms in women include a painful or burning sensation when urinating or a yellowish vaginal discharge. More advanced symptoms include abdominal pain, bleeding between menstrual periods, vomiting, or fever.

Men usually have a whitish-yellowish discharge from the penis and a burning sensation during urination that may be severe. Symptoms of rectal infection include anal itching, and sometimes painful bowel movements.

Diagnosis of gonorrhea ???

Testing for gonorrhea is done by swabbing the infected site and culturing the bacteria on the swab in the laboratory. The culture is positive when the gonorrhea bacteria are found to be growing on a culture plate. A newer test can detect both gonorrhea and chlamydia in a urine sample. Up to 40% of women with gonorrhea are also infected with chlamydia.

How silent is it ???

Gonorrhea is often silent in women. Over half of infected women have no symptoms in the early stages of gonorrheal infection. If symptoms do occur, there may be burning on urination, frequent urination, yellowish vaginal discharge, redness of the genitals, swelling of the genitals, and a burning or itching of the vaginal area.

Treatment ?????

Because a high proportion of men and women who have gonorrhea also have chlamydia, the goal of treatment is to cure both infections. Your partner(s) should be treated at the same time you are.

Treatment for uncomplicated gonorrhea consists of antibiotics, including ceftriaxone, cefixime, ciprofloxacin, or ofloxacin for gonorrhea along with azithromycin, doxycycline, or erythromycin for chlamydia.

Prevention Of Gonorrhea ???

All sexually active persons should consider using latex condoms to prevent STDs and HIV infection, even if they are using another form of contraception. Latex condoms used consistently and correctly are an effective means for preventing disease (and pregnancy). Talk openly with your partner about STDs, HIV, and hepatitis B infection, and the use of contraception.

Can i treat a Pregnant woman with Gonorrhea ????

If you become infected with gonorrhea while you are pregnant, it is important that you seek treatment quickly. Not only is it possible to transmit the infection to your child during childbirth, but this common sexually transmitted disease can also cause complications in your pregnancy.

Questions U can ask ur Family Doctor!!!

1. Should the sexual partner be alerted so that they can be tested?
2. Has the gonorrhea progressed into Pelvic Inflammatory Disease (PID)?
3. Can the gonorrhea come back without additional exposure?
4. Do any of the internal contraceptive gels, ointments, devices, etc. help prevent gonorrhea?
5. What type of medication will you be prescribing?
6. Are there any side effects?
7. Can I tell if a sexual partner has gonorrhea before having sexual intercourse?

From My Personal Experience  !!!

Narcotics have been a heavy substance at present in the international market . And wit me being Indian , Im proud India is a bit brilliant in narcotic issues . narcotics are Less told and More sold here . I being a reasearcher of Medicine was also a occasional user of narcotics during my college days . But the glamour behind the story is ……………i Lost interest , sorry i lost my personality at first then my character a bit tooo…..Its not just that there are more harms ……Frankly speakin i have had just some weed bfore and thats not the end …..i was a occasional user too . I had a gr8 fren from US who use to do most of the drugs on the plane. But now he has stopped all ….not bcoz he was told to , He realized and changed a lot ……………….All bcoz of a guy we met in the streets ….he was a middleaged man from souther parts of India …he wore a dress wit rags and rails all over it …….he had a body lookin lean like a Anorexia patient …….then he stood some 6 ft tall from the ground ………….and was talkin in english to my suprise ….bcoz he looked more bad than a normal Beggar in the country …..i asked him where are u from …..he quickly answered “can i have some money !!! some 10 rs will do ” ……….on those days we lived bachelor lives (no money but waiting for honey ) ……But still i paid a sum of 20 to him he said thanks happily …………….and then said his story…………………….He was Mr.X a son of a very famous businessman in the state of kerala ………he was 38 at that time …………..he has spend almost all the money which his father has left behind by the help of a few bad frens ……………… he was 20 when he was drugged first wit the help of few frens ……..then he was obsessed wit it when he was just 21 and he has been a regular drug addict from that day …….He has lost his frstrated father when he was 24 and then had no good marks to passs………….failed in studies …….got married at 28 ……failed in marriage when he was 30 doubting on his beautiful and tolerating wife ………………………no kids too………..failed in money making and had no money to save …………..got loans from almost all the banmks and atlast was in road………………..he has lost everything in his life including his mother but has gained a lot a bad names ………..After having a small chat wit him …..we came home and my fren like almost cried and told me he will never use drugs again in his life ……………And atlast he did it STOPPED EVERYTHING !!!!!!!!!!!!……………………ALL THE DRUGS HE KNEW……AND NOW HE IS A SUCESSFUL DOCS IN THE US…………………………….so i please advice u people who have finished reading the entire issue to stop any narcotic drugs u are abused to……….plZ FRENS ….

DEFINITION????

An addictive drug, such as opium, that reduces pain, alters mood and behavior, and usually induces sleep or stupor. Natural and synthetic narcotics are used in medicine to control pain.

HISTORY???

Narcotics are the oldest as well as the strongest analgesics, or pain-relieving drugs, known to humans. Ancient Sumerian and Egyptian medical texts dated as early as 4000 B.C. mention the opium poppy (Papaver somniferum) as the source of a milky fluid (opium latex) that could be given to relieve coughs and insomnia as well as ease pain. Traditional Chinese medicine recommended the opium poppy, known to Chinese physicians as ying su ke, for the treatment of asthma, severe diarrhea, and dysentery as well as chronic pain and insomnia. Opium latex contains between 10 and 20 percent morphine, which in its purified form is a white crystalline powder with a bitter taste.

Narcotics are central nervous system depressants that produce a stuporous state in the person who takes them. These drugs often induce a state of euphoria or feeling of extreme well-being, and they are powerfully addictive. The body quickly builds a tolerance to narcotics in as little as two to three days, so that greater doses are required to achieve the same effect. Because of the addictive qualities of these drugs, most countries in the twenty-first century have strict laws regarding the production and distribution of narcotics. These laws became necessary when opium addiction in the nineteenth century became a widespread social problem in the developed countries. Opium, which was the first of the opioids to be widely used, had been a common folk remedy for centuries that often led to addiction for the user; in fact, many popular Victorian patent medicines for “female complaints” actually contained opium. The invention of the hypodermic needle in the mid-nineteenth century, however, increased the number of addicts because it allowed opioids to be delivered directly into the bloodstream, thereby dramatically increasing their effect.

TYPES???

As of the early 2000s, narcotics are commonly classified into three groups according to their origin:

• Natural derivatives of opium: Narcotics in this group include morphine itself and codeine.
• Partially synthetic drugs derived from morphine: These drugs include heroin, oxycodone (OxyContin), hydromorphone (Dilaudid), and oxymorphone (Numorphan).
• Synthetic compounds that resemble morphine in their chemical structure: Narcotics in this group include fentanyl (Duragesic), levorphanol (Levo-Dromoran), meperidine (Demerol), methadone, and propoxyphene (Darvon).

Narcotics are available in many different forms, ranging from oral, intramuscular, and intravenous preparations to patches that can be applied to the skin (fentanyl). Illegal street heroin can be taken by inhalation as well as by injection.

EFFECTS??????

Drug effects depend heavily on the dose, route of administration, previous exposure to the drug, and the expectation of the user. Aside from their clinical use in the treatment of pain, cough suppression and acute diarrhea, narcotics produce a general sense of well-being known as euphoria by reducing tension, anxiety, and aggression. These effects are helpful in a therapeutic setting and contribute to their popularity as recreational drugs, as well as helping to produce dependency.

Narcotic use is associated with a variety of effects including drowsiness, itching, sleeplessness, inability to concentrate, apathy, lessened physical activity, constriction of the pupils, dilation of the subcutaneous blood vessels causing flushing of the face and neck, constipation, nausea and vomiting and, most significantly, respiratory depression. As the dose is increased, the subjective, analgesic, and toxic effects become more pronounced. Except in cases of acute intoxication, there is no loss of motor coordination or slurred speech as occurs with many depressants.

effects of meth a narcotic drug

ASSOCIATED PROBLEMS ?????

AIDS, Addiction, Cocaine, Controlled Substances Act, Greek, HIV, Hard and soft drugs, Heroin, Narcissus, Narcoterrorism, Narcotics Anonymous, Opioids, Pethidine/Meperidine, U.S., aggression, analgesia, anxiety, coca, contaminants, drug legalization, endocarditis, euphoria, hepatitis, heroin, legalization, morphine, nitrogen, nitrogen narcosis, opioid, opium, scuba diving, sedation, syringes…

POSITIVE EFFECTS????????

For severe episodes of low back pain, narcotic pain medications may be prescribed. Clearly, narcotic agents are strong and potentially addictive forms of medication and should only be administered by a physician.

All narcotic agents have a dissociative effect that helps patients manage pain. It does not actually deaden the pain, but works to dissociate patients from the pain. Commonly used narcotics, listed in ascending order of potency (strength) include:

• codeine (e.g. Tylenol #3)
• propoxyphene (e.g. Darvocet)
• hydrocodone (e.g. Vicodin)
• oxycodone (e.g. Percocet, Oxycontin)

HOW CAN I FORGET MORPHINE ????

Morphine is used to treat moderate to severe pain. It works by dulling the pain perception center in the brain. Short-acting formulations are taken as needed for pain. Extended-release formulations are used when around-the-clock pain relief is needed. Morphine is not for treating pain just after surgery unless you were already taking it before the surgery.

Before using morphine, tell your doctor if you are allergic to any drugs, or if you have:

• asthma, COPD, sleep apnea, or other breathing disorders;
• liver or kidney disease;
• underactive thyroid;
• curvature of the spine;
• a history of head injury or brain tumor;
• epilepsy or other seizure disorder;
• low blood pressure;
• gallbladder disease;
• Addison’s disease or other adrenal gland disorders;
• enlarged prostate, urination problems;
• mental illness; or
• a history of drug or alcohol addiction.

These effects include, but are not limited to:

• Pain relief
• Cough suppression
• Drowsiness
• Anxiety relief
• Unusual unpleasant feelings (dysphoria) or unusual pleasant feelings (euphoria)
• Decreased breathing (slow or shallow breathing)
• Certain changes in the circulatory system
• Slowing of the digestive tract
• Release of histamine (which often causes itching)
• Physical dependence.

(See Morphine Uses for more information.)

MORPHINE SIDEFFECTS !!

As with any medicine, morphine can cause side effects. However, not everyone who takes the drug will experience side effects. Most people tolerate it quite well. If side effects do occur, in most cases, they are minor and either require no treatment or are easily treated by you or your healthcare provider. Serious side effects are less common.

Common side effects of this drug include, but are not limited to:

• Lightheadedness or dizziness
• Drowsiness
• Nausea or vomiting
• Sweating
• An unusual unpleasant feeling (dysphoria) or an unusual pleasant feeling (euphoria)
• Constipation

SIGNS AND SYMPTOMS OF NARCOTIC USE

Narcotics users can develop tolerance, as well as psychological and physical dependence to opioids when they take them over an extended period of time.

• Tolerance refers to a decreased response to a drug, with increasing doses required to achieve comparable effects.

• Psychological dependence refers to compulsive drug use in which a person uses the drug for personal satisfaction, often in spite of knowing the health risks.

• Physical dependence occurs when a person stops using the narcotic but experiences a withdrawal syndrome (or set of symptoms).

• Signs and symptoms of narcotic abuse
  • analgesia (feeling no pain),

• • sedation,

• • euphoria,

• • respiratory depression (shallow breathing),

• • small pupils, bloodshot eyes,

• • nausea, vomiting,

• • itching skin, flushed skin,

• • constipation,

• • slurred speech,

• • confusion, poor judgment, and

• • needle marks on the skin

WITHDRAWAL EFFECTS OF NARCOTIC USE !!!!!

• Signs and symptoms of narcotic withdrawal: The withdrawal syndrome from narcotics generally includes signs and symptoms opposite of the drug’s intended medical effects. The severity of the withdrawal syndrome increases as the drug dose increases. The longer the duration of the physical dependence to the narcotic increases, the more severe the withdrawal syndrome. Symptoms of heroin withdrawal generally appear 12-14 hours after the last dose. Symptoms of methadone withdrawal appear 24-36 hours after the last dose. Heroin withdrawal peaks within 36-72 hours and may last seven to 14 days. Methadone withdrawal peaks at three to five days and may last three to four weeks. Although uncomfortable, acute narcotic withdrawal for adults is not considered life-threatening unless the person has a medical condition that compromises their health (for example, if someone has severe heart disease). Some of the signs and symptoms of narcotic withdrawal are listed below:
  • Anxiety

• • Irritability

• • Craving for the drug

• • Increased respiratory rate (rapid breathing)

• • Yawning

• • Runny nose

• • Salivation

• • Gooseflesh

• • Nasal stuffiness

• • Muscle aches

• • Nausea or vomiting

• • Abdominal cramping

• • Diarrhea

• • Sweating

• • Confusion

• • Enlarged pupils

• • Tremors

• • Lack of appetite

COMPLICATIONS ????

• Signs and symptoms of narcotic withdrawal: The withdrawal syndrome from narcotics generally includes signs and symptoms opposite of the drug’s intended medical effects. The severity of the withdrawal syndrome increases as the drug dose increases. The longer the duration of the physical dependence to the narcotic increases, the more severe the withdrawal syndrome. Symptoms of heroin withdrawal generally appear 12-14 hours after the last dose. Symptoms of methadone withdrawal appear 24-36 hours after the last dose. Heroin withdrawal peaks within 36-72 hours and may last seven to 14 days. Methadone withdrawal peaks at three to five days and may last three to four weeks. Although uncomfortable, acute narcotic withdrawal for adults is not considered life-threatening unless the person has a medical condition that compromises their health (for example, if someone has severe heart disease). Some of the signs and symptoms of narcotic withdrawal are listed below:
  • Anxiety

• • Irritability

• • Craving for the drug

• • Increased respiratory rate (rapid breathing)

• • Yawning

• • Runny nose

• • Salivation

• • Gooseflesh

• • Nasal stuffiness

• • Muscle aches

• • Nausea or vomiting

• • Abdominal cramping

• • Diarrhea

• • Sweating

• • Confusion

• • Enlarged pupils

• • Tremors

• • Lack of appetite

NARCOTICS IN PREGNANT WOMAN !!!

A retrospective analysis has been made of the outcome of pregnancy in 174 women abusing narcotics, managed by a specialist team from a drug-dependency antenatal clinic. These women were cared for through 182 pregnancies of greater than 20 weeks’ gestation, resulting in 183 live and 5 stillbirths. The majority of patients were enrolled in a methadone programme and stabilized on the drug before the third trimester. The group was characterized by a high prevalence of previous obstetric and medical problems. The most common antenatal complications were preterm labour (24%) and anaemia (12%). Preterm delivery and small-for-gestational-age each occurred in a quarter of pregnancies. The mean birth-weight for the group was 2,746 g +/- 721 g; mean +/- S.D. Eight perinatal deaths occurred (5 stillbirths, 3 neonatal deaths), giving a perinatal mortality rate of 43/1,000. The data on narcotic abusers have been compared with similar data obtained from randomly selected public antenatal clinic patients who delivered during the same period.

FATAL EFFECTS OF NARCOTICS

Respiratory arrest is a common cause of death from cocaine overdose. It is more likely to occur if a depressant drug such as heroin has also been taken. Death can also result from events as varied as abnormal rhythms of the heart, ruptured blood vessels, very high body temperature, and gangrene of the intestine.Although most deaths have followed intravenous injection, they have also occurred after smoking, snorting, or oral use. The lethal dose of cocaine is not known, but is probably quite variable. Death has resulted from doses as low as 30 mg snorted and 20 mg injected, yet users have survived doses of several grams (several thousand milligrams). Virtually no dose, no matter how small, can be guaranteed safe. Impurities in street cocaine can also produce fatal allergic reactions.

MJ\’s fatal drug overdose

Garth Prison durgs

WAT IS IT????

Stroke is a disease that affects the arteries leading to and within the brain. It is the No. 3 cause of death in the United States, behind diseases of the heart and cancer. A stroke occurs when a blood vessel that carries oxygen and nutrients to the brain is either blocked by a clot or bursts. When that happens, part of the brain cannot get the blood (and oxygen) it needs, so it starts to die.

Is it similar to brain hemorrhage ???

Brain Hemorrhage is a condition caused due to a sudden stroke to a person after blood leaks out from the blood vessels in the brain. This situation occurs due to the break in the wall of blood vessel, the blood spills out of the blood vessel and enters the area where vital tissues and cells of brain reside, killing those tissues and cells; this causes the patient to become seriously ill and needs immediate medication/treatment.

Symptoms ???

Symptoms

If you have symptoms of a stroke, seek emergency medical care. General symptoms of a stroke include:

• Sudden numbness, paralysis, or weakness in your face, arm, or leg, especially on only one side of your body.
• New problems with walking or balance.
• Sudden vision changes.
• Drooling or slurred speech.
• New problems speaking or understanding simple statements, or feeling confused.
• A sudden, severe headache that is different from past headaches.

Symptoms vary depending on whether the stroke is caused by a clot or bleeding. The location of the blood clot or bleeding and the extent of brain damage can also affect symptoms.

1)Symptoms of an ischemic stroke (caused by a clot blocking a blood vessel) usually occur in the side of the body opposite from the side of the brain where the clot occurred. For example, a stroke in the right side of the brain affects the left side of the body.

2)Symptoms of a hemorrhagic stroke (caused by bleeding in the brain) can be similar to those of an ischemic stroke but may be distinguished by symptoms relating to higher pressure in the brain, including severe headache, nausea and vomiting, neck stiffness, dizziness, seizures, irritability, confusion, and possibly unconsciousness.

Symptoms of a stroke may progress over minutes, hours, or days, often in a stepwise fashion. For example, mild weakness may progress to an inability to move the arm and leg on one side of the body.

• If a stroke is caused by a large blood clot (ischemic stroke) or bleeding (hemorrhagic stroke), symptoms occur suddenly, within seconds.
• When an artery that is narrowed by atherosclerosis becomes blocked, stroke symptoms usually develop gradually over minutes to hours, or (in rare cases) days.
• If several smaller strokes occur over time, the person may have a more gradual change in walking, balance, thinking, or behavior (multi-infarct dementia).

It is not always easy for people to recognize symptoms of a small stroke. They may mistakenly think the symptoms can be attributed to aging, or the symptoms may be confused with those of other conditions that cause similar symptoms.

Risk Factors??

1)Controllable

• Hypertension
• Atrial Fibrillation
• High Cholesterol
• Diabetes Mellitus
• Smoking and Tobacco chewing
• Alcohol Use
• Obesity or Overweight

2)Non- controllable

• Age >55
• Gender – Males most common , but more women die of stroke
• Race – African American>Hispanic>Asians>caucasions
• Family History
• Previous Stroke or Transient Ischemic attacks or Thrombosis or Embolism

What Are the Types of Stroke?

Stroke can be caused either by a clot obstructing the flow of blood to the brain (called an ischemic stroke) or by a blood vessel rupturing and preventing blood flow to the brain (called a hemorrhagic stroke).

Diagnosis of Stroke??

When someone has shown symptoms of a stroke or a TIA (transient ischemic attack or mini stroke), a doctor will gather information and make a diagnosis. A doctor may use many different tests. The ones listed here are just some of the more common options.

Treatment !!!!

Ischemic Stroke

Acute Treatment

• Clot busters, e.g., tPA
  The most promising treatment for ischemic stroke is the FDA-approved clot-busting drug tPA (tissue plasminogen activator), which must be administered within a three-hour window from the onset of symptoms to work best. Administering tPA or other clot-dissolving agents is complex and is done through an intravenous (IV) line in the arm by hospital personnel. If given promptly, tPA can significantly reduce the effects of stroke and reduce permanent disability. Generally, only 3 to 5 percent of those who suffer a stroke reach the hospital in time to be considered for this treatment.

Preventive Treatment

• 	Click to enlarge

  Anticoagulants/Antiplatelets
  Antiplatelet agents such as aspirin and anticoagulants such as warfarin interfere with the blood’s ability to clot and can play an important role in preventing stroke. click here for  anticoagulants.

• Carotid Endarterectomy
  Carotid endarterectomy is a procedure in which blood vessel blockage is surgically removed from the carotid artery. View a detailed illustration of carotid endarterectomy.

• Angioplasty/Stents
  Doctors sometimes use balloon angioplasty and implantable steel screens called stents to treat cardiovascular disease and reduce fatty buildup clogging a vessel. View a detailed illustration of carotid stent.

Hemorrhagic Stroke (Subarachnoid hemorrhage or AVM)

• Surgical Intervention
  For hemorrhagic stroke (specifically for a subarachnoid hemorrhage), surgical treatment is often recommended to either place a metal clip at the base, called the neck, of the aneurysm or to remove the abnormal vessels comprising an arteriovenous malformation (AVM). Learn more about AVM.

• Endovascular Procedures, e.g., “coils”
  Endovascular procedures are less invasive and involve the use of a catheter introduced through a major artery in the leg or arm, guided to the aneurysm or AVM where it deposits a mechanical agent, such as a coil, to prevent rupture. (wat is  aneurysms).

What is Heart Attack

INTRODUCTION

A heart attack (also called “myocardial infarction”) occurs when a blood vessel supplying blood to a part of the heart becomes blocked, resulting in permanent damage to the heart muscle due to the lack of blood flow. The blood vessel can become blocked from advancing atherosclerotic plaque lesions, a sudden formation of a blood clot, or from the spasming of a coronary artery – an artery that supplies blood to the heart.

Most people believe that a heart attack is caused by a slow, progressive build-up of plaque, comforting themselves that it takes a lifetime to become completely clogged – but this just isn’t true for a majority of heart attacks. Heart specialists now believe that most heart attacks occur when an unstable, atherosclerotic plaque lesion, filled with cholesterol and fat, suddenly breaks apart, thus forming an open wound within the artery wall. Blood platelets and clotting proteins rush to the wound and form a clot — called a thrombus. The clot can enlarge in a matter of moments, causing obstruction of blood flow to the heart with resultant angina (chest pain). If the blood flow becomes completely obstructed, a heart attack ensues.

Surprisingly, it is the small plaques that can be the most lethal. A person with a 50% blockage who suddenly becomes obstructed is at much greater risk of having a large amount of heart damage than a person with a slowly progressive blockage. A person with a 90% blockage that was slow to progress has probably had a chance to develop “collaterals”–– smaller blood vessels that grow to take over the job of the big vessel that has been gradually closing down.

Is it an Emergency ?????

Every Second Counts
A heart attack is a life–threatening event. With immediate medical intervention — preferably within the first hour of onset of symptoms – heart damage may be averted or reduced. A new blood test measuring “troponin” – a chemical released into the blood during a heart attack – allows doctors to diagnose a heart attack more quickly and accurately than ever before. Time equals muscle is the theme that resounds in emergency rooms and treatment is aimed at quickly restoring blood flow to the heart muscle to prevent permanent damage.

Risk Factors ????

1) Increased LDL/HDL ratios (i.e.,, elevated LDL and low HDL levels)Cholesterol

2) Smoking

3) Diabetes

4) Hypertension

5) Obesity

6)  Stress (i.e., stress or depression)

7) Failure to eat fruits and vegetables daily

Failure to Exercise

9) Failure to drink Moderate Alcohol (complex relationship between alcohol and the heart.)

10) Metabolic syndrome.

11) Increased CRP ( C reactive Protein)

12) Taking Birth Control Pills

13) Complicated Pregnancy

Non modifiable Risk factors?????????

• A family history of premature CAD (generally, CAD that has occurred in male relatives before the age of 50, or in female relatives before the age of 60.)
• Age 55 or older (men), or 65 or older (women)
• For women, being post-menopausal, or having your ovaries removed.
• Chronic kidney disease.

Is there a recent rise Of Heart Attack patients in INDIA???

Yes Bcoz of the Follwing Reasons :

1. Economic Progress

2. Better standard living

3. Westernisation

4. Change of food habits

5. More prone genetics

6. Small vessel Coronary Artery Disease

7. High incidence of Diabetes

8. More Smokers

Symptoms ?????

A unique fact about heart disease is that, in general, the more serious the condition the more remote from the heart are the symptoms.   Amongst danger signals that may, but not necessarily do, betoken heart disease and invite prompt medical attention are:

1 Shortness of breath after slight exertion.

2  Pain or tightness in the chest, often running down the left arm.

3  Swelling in the ankles and abdomen.

4  Dizziness, light-headedness, or vertigo.

5  Seeing double (a particularly dangerous sign).

6  Indigestion that is vague and hangs on.

7  Persistent head-ache.

8  Fatigue without otherwise explained origin.

SIGNS?????

• Bradycardia to Tachycardia
• Angina
• Arrythmia
• Low cardiac Output
• Rales in case of Pulmonary edema
• Cyanosis
• Cold extremities

DIAGNOSIS ???

Essentials of Diagnosis

• Sudden but not instantaneous development of prolonged (> 30 minutes) anterior chest discomfort (sometimes felt as “gas” or pressure) that may produce arrhythmias, hypotension, shock, or cardiac failure.
• Sometimes painless, masquerading as acute CHF, syncope, stroke, or shock.
• ECG: ST-segment elevation or depression, evolving Q waves, symmetric inversion of T waves.
• Elevation of cardiac markers (CK-MB, troponin T, or troponin I).
• Appearance of segmental wall motion abnormality by imaging techniques.

Treatment ????

1)Aspirin and Clopidogrel All patients with definite or suspected myocardial infarction should receive aspirin at a dose of 162 mg or 325 mg at once regardless of whether thrombolytic therapy is being considered or the patient has been taking aspirin. Chewable aspirin provides more rapid blood levels. Patients with a definite aspirin allergy should be treated with clopidogrel; a 300 mg (or 600 mg) loading dose will result in faster onset of action than the standard 75 mg dose.

2) Thrombolytic Therapy: Streptokinase is not commonly used for treatment of acute myocardial infarction since it is less effective at opening occluded arteries and less effective at reducing mortality. It is non-fibrin-specific, causes depletion of circulating fibrinogen, and has a tendency to induce hypotension, particularly if infused rapidly. This can be managed by slowing or interrupting the infusion and administering fluids. There is controversy as to whether adjunctive heparin is beneficial in patients given streptokinase, unlike its administration with the more clot-specific agents. Allergic reactions, including anaphylaxis, occur in 1–2% of patients, and this agent should generally not be administered to patients with prior exposure.

3) Nitrates: Nitroglycerin is the agent of choice for continued or recurrent ischemic pain and is useful in lowering BP or relieving pulmonary congestion. However, routine nitrate administration is not recommended, since no improvement in outcome has been observed in the ISIS-4 or GISSI-3 trials, in which a total of over 70,000 patients were randomized to nitrate treatment or placebo. Nitrates should be avoided in patients who received phosphodiesterase inhibitors (sildenafil, vardenafil, and tadalafil) in the prior 24 hours.

4) Beta Blockers  : Although trials have shown modest short-term benefit from intravenous -blockers given immediately after acute myocardial infarction, it has not been clear that this provides a major advantage over simply beginning an oral -blocker. The Chinese COMMIT/CCS-2 trial involving 45,000 patients found no overall benefit to intravenous followed by oral metoprolol; the aggressive dosing (three 5 mg intravenous boluses followed by 200 mg/d orally) appeared to prevent reinfarction at the cost of increasing shock in patients presenting with heart failure. Thus, -blockade should be avoided in patients with decompensated heart failure, decompensated asthma, or high degrees of AV block. The CAPRICORN trial showed the benefits of carvedilol following the acute phase of large myocardial infarction with contemporary care.

5)ACE Inhibitors: A series of trials (SAVE, AIRE, SMILE, TRACE, GISSI-III, and ISIS-4) have shown both short- and long-term improvement in survival with ACE inhibitor therapy. The benefits are greatest in patients with low EFs, large infarctions, or clinical evidence of heart failure. Because substantial amounts of the survival benefit occur on the first day, ACE inhibitor treatment should be commenced early in patients without hypotension, especially patients with large or anterior myocardial infarction.

6) Calcium Channel Blockers : There are no studies to support the use of calcium channel blockers in most acute myocardial infarction patients—and indeed, they have the potential to exacerbate ischemia and cause death from reflex tachycardia or myocardial depression. One exception is that diltiazem and verapamil appear to prevent reinfarction and ischemia in the subset of patients with non-Q wave infarction. Diltiazem is preferable because it causes less myocardial depression. The dosage is 240–360 mg daily. Otherwise, long-acting calcium channel blockers should be reserved for management of hypertension or ischemia as second- or third-line drugs after -blockers and nitrates

7) Surgery:

Prevention>>>

How Can a Heart Attack Be Prevented?

Lowering your risk factors for coronary artery disease (CAD) can help you prevent a heart attack. (See “Who Is At Risk for a Heart Attack?“) Even if you already have CAD, you can still take steps to lower your risk of heart attack.

Reducing the risk of heart attack usually means making healthy lifestyle choices. You also may need treatment for medical conditions that raise your risk.

Healthy Lifestyle Choices

Healthy lifestyle choices to help prevent heart attack include:

• Following a low-fat diet rich in fruits and vegetables. Pay careful attention to the amounts and types of fat in your diet. Lower your salt intake. These changes can help lower high blood pressure and high blood cholesterol.
• Losing weight if you’re overweight or obese.
• Quitting smoking.
• Doing physical activity to improve heart fitness. Ask your doctor how much and what kinds of physical activity are safe for you.

Treat Related Conditions

In addition to making lifestyle changes, you can help prevent heart attacks by treating conditions you have that make a heart attack more likely:

• High blood cholesterol. You may need medicine to lower your cholesterol if diet and exercise aren’t enough.
• High blood pressure. You may need medicine to keep your blood pressure under control.
• Diabetes (high blood sugar). If you have diabetes, control your blood sugar levels through diet and physical activity (as your doctor recommends). If needed, take medicine as prescribed.

Have an Emergency Action Plan

Make sure that you have an emergency action plan in case you or someone else in your family has a heart attack. This is especially important if you’re at high risk or have already had a heart attack.

Talk with your doctor about the signs and symptoms of heart attack, when you should call 9–1–1, and steps you can take while waiting for medical help to arrive.

INTRODUCTION

In each menstrual cycle, follicles grow on the ovaries. Eggs develop within those follicles, one of which will reach maturity faster than the others and be released into the fallopian tubes. This is “ovulation”. The remaining follicles will degenerate.

In the case of polycystic ovaries, however, the ovaries are larger than normal, and there are a series of undeveloped follicles that appear in clumps, somewhat like a bunch of grapes. Polycystic ovaries are not especially troublesome and may not even affect your fertility.

However, when the cysts cause a hormonal imbalance, a pattern of symptoms may develop. This pattern of symptoms is called a syndrome. These symptoms are the difference between suffering from polycystic ovary syndrome and from polycystic ovaries.

How common in PCOS???

Polycystic ovary syndrome is the most common hormonal disorder occurring in women during their reproductive years. It’s thought that 4% to 10% of all women have the disorder. However, since many women don’t know they have polycystic ovarian syndrome or some aspect of it, the actual number probably exceeds 10%. Polycystic ovarian syndrome is one of the leading causes of infertility. Symptoms frequently start to show up soon after puberty.

Causes????

There is disagreement and uncertainty as to what causes polycystic ovarian disease. Polycystic ovaries and polycystic ovary syndrome have been associated with one or more of these factors:

• Genetic predisposition.
• Insulin resistance or hyperinsulinism (high blood levels of insulin).
• Obesity.
• Hyperandrogenism (excessive production of male hormones).
• Abnormality of the hypothalamic-pituitary-gonadal axis (organ/hormonal disorder).
• Environmental chemical pollution (hormonal disruptors)
• Food adulterantion (excitatory amino acids, for example)
• Chronic inflammation.

Some of these causal factors may also be consequences of polycystic ovary disease. In other words, we have an amazingly complex network of interacting variables, each of which influences the other. Polycystic ovarian syndrome is not a simple disease with a single cause.

The Natural Diet Solution for PCOS and Infertility describes the possible causes of polycystic ovary syndrome in great detail.

Symptoms???

Polycystic ovarian syndrome presents a complex and baffling array of symptoms, consisting of some combination of the following symptoms that vary with each individual:

• Multiple ovarian cysts
• Irregular or absent menses
• Infertility
• Acne
• Obesity or inability to lose weight
• Excessive body or facial hair (hirsutism)
• Insulin resistance and possibly diabetes
• Thinning of scalp hair
• Velvety, hyperpigmented skin folds (acanthosis nigricans)
• High blood pressure
• Polycystic ovaries that are 2-5 times larger than healthy ovaries.
• Multiple hormone imbalances, commonly including:
  • Androgens (testosterone)
  • Cortisol
  • Estrogens
  • FSH (follicle stimulating hormone)
  • Insulin.
  • LH (luteinizing hormone)
  • progesterone
  • Prolactin.
  • Thyroid hormones.
• Impaired lung function.
• Sleep apnea.
• Fatty liver degeneration (NAFLD).
• Depression

Treatment ????

The first PCOS treatment for Infertility is usually the administration of medications to stimulate ovulation.

Clomiphene citrate (Clomid or Serophene)

An oral fertility drug used to stimulate ovulation, correct ovulation process, to improve egg production and to fix luteal phase deficiency. The drug is taken for five days early in the menstrual cycle. Clomid may become futile with a long use, for more than six cycles.

With some evidence, it has been stated that continual use of the drug, for twelve or more cycles, may increase the risk of ovarian cancer.

Metformin (Glucophage)

It is an insulin-sensitizing agent used to induce ovulation. Common Metformin medications include, Generic Metformin Hcl, Glucophage, and Glucophage XR. If Clomid fails to ovulate, a combination of “Metformin” and “Clomid” is taken as a PCOS treatment drugs for infertility.

The medication ‘Metformin’ increases the fertility by improving the effectiveness of the insulin while decreasing the insulin levels and in turn androgen levels. Normalizing the androgen levels enhances the natural ovulation.

hCG (human chorionic gonadotrophin) (Profasi)

An intramuscular injection used in conjunction with Clomid. The effect of hCG on follicle is same as LH (luteinizing hormone). HCG stimulates the follicle to release its egg (ovulate) approximately 36 hours later.Ovulation may be blocked, when hCG is taken too early. Ovarian hyper stimulation and cyst formation can result with too much hCG usage.The other commonly used PCOS treatment drugs for infertility include hMG (human menopausal gonadotrophin), FSH (follicle stimulating hormone), GnRH (gonadotrophin releasing hormone), GnRHa (GnRH analogs) and Prolactin inhibition drugs.

PCOS Treatment For Infertility – Medical Procedures

IUI (intrauterine insemination)

A basic PCOS treatment for women with infertility problem is intrauterine insemination, also known as Artificial Insemination. It is a fast and painless medical procedure where the male partner’s sperm is introduced directly into the female’s uterus (intrauterine) for the purpose of conception.

The procedure is usually done in conjunction with the ovarian stimulation drugs because regular menstrual cycle and healthy ovulation makes conception very successful.

IVF (in-vitro fertilization)

A simpler, safer and more successful PCOS treatment option to induce ovulation in infertile women is in vitro fertilization. The procedure involves the removal of eggs from female partner’s body and fertilizing them with the sperm of male partner.

The embryo (fertilized egg) is then introduced into the uterus (womb). Ovarian stimulation drugs (hCG, hMG, FSH or progesterone) are used to stimulate the ovaries to produce fertilizable oocytes (eggs).GIFT (Gamete Intra Fallopian Transfer), ICSI (Intracytoplasmic Sperm Injection) are the medical procedures of PCOS treatment for infertile women.The success rate of PCOS treatment options to induce ovulation depends on the age of the woman, the type of ovarian stimulation medication, and other factors that contribute to infertility in the woman.

Yoga asans that help PCOS???

Down the years, it has been found that Yoga is the only recourse left to PCOD / PCOS sufferers. Yoga is a holistic science and art of living. This is because routines Yoga consisting of asanas (poses), pranayamas (breathing techniques) and kriyas (cleansing exercises) prescribed in Yoga help tone up the whole system. There are certain fixed Yoga asanas (poses) like the sitting, standing and supine poses that haven proven to greatly help PCOD / PCOS patients. In general, the Yoga program for PCOD / PCOS is as follows:

• A series of Yoga asanas (poses). While there is no exact pose or exercise that is known to help heal PCOD / PCOS, experience tells us that some of the poses – if done regularly – sitting, standing and lying on the back, over time yield the desired results. But, you should make sure to avoid all the inverted poses.
• Practice lots of Pranayamas (Breathing Exercises) in a slow, unhurried, relaxed rhythm. You may breathe at your own slow pace, or inhale and exhale to the count of 3 or 4. But do this very slowly and avoid straining or putting pressure on your lungs. The recommended pranayamas (breathing exercises) for PCOD / PCOS women are Mild Kapalabhatti (Skull Cleansing), Anuloma-Viloma (Alternate Nostril Breathing) and Ujjayi (Ocean Breath).
• You should also practise Nispanda Bhava (Unmoving Observation) and Shavasana (Corpse pose) 2 – 3 times every day. These will definitely help since PCOD / PCOS victims are, by and large, tense and stressed out. Subsequently, they need plenty of relaxation.
• Finally, let your diet be Yogic and Sattvic. This essentially means pure and predominantly vegetarian, with lots of seasonal fruits, sprouts, fresh salads and dried fruits. Steer clear of milk and milk products, particularly cheeses and butter, all confectionery products, fatty, fried and spicy foods, cigarettes and alcohol
• Likewise, avoid stress and tension, so try and avoid all stressful situations. Even if difficult, you will find that taking the trouble and making a few short term sacrifices will benefit you enormously in the long run.