Is a Cyst on the Ovary One of the Early Symptoms of Ovarian Cancer? Do Not Wait – Find Out Now!

Having a cyst on ovary produces very vague signs of illness or problems, unless of course you are fortunate (?) enough to have the stabbing pain in your abdomen or pelvis, (ovary pain) which can sometimes be a meaningful sign that it is time to give your gynecologist a call and schedule a pelvic examination. Unfortunately, pain or pressure in your lower stomach area is one of the early symptoms of ovarian cancer, as well.

Does an ovarian cyst naturally mean you have ovarian cancer? No…absolutely not. Could the cyst actually be malignant…in other words…cancer of the ovaries? Regrettably, yes! Ovarian cyst symptoms need to be treated very seriously, even though the majority of them are nothing to be concerned about. Cysts that do not ever become cancer are functional cysts, and occur many times without any symptoms at all.

A type of cyst on ovary that can be cancerous is a dermoid cyst, but only one to two percent actually are malignant. Cysts on ovaries actually can one of the ONLY early symptoms of ovarian cancer that is not a vague, generic sign.

So, what are some of the early symptoms of ovarian cancer, or for that matter…a cyst on ovary?

– pain in the lower abdomen
– irregular menstrual periods/bleeding in between periods
– bloating, or pressure in the abdomen
– difficulty breathing
– gastrointestinal problems…nausea, change in bowel habits, indigestion
– back pain
– feeling full quickly/not hungry
– unexplained weight gain/weight loss
– fatigue
– fever
– urinary problems

Ovarian cancer produces many obscure symptoms that might manifest and can very easily be misinterpreted for a more common illness. There have been studies done though, that have indicated that having MORE than one of these symptoms for a prolonged period…four or five weeks…is definitely a reason to see your doctor.

Because there really are no telltale early symptoms of ovarian cancer, other than some of the above signs…a woman must pay close attention to what she is experiencing. If there is any suspicion whatsoever that a cyst on ovary is present and that the patient feels her doctor is not doing enough, the best solution is to…get a second opinion. It is your life…take charge of it!

Remedies for Thrush in Adults – 3 Simple Tips to Erase Adult Thrush Naturally

Thrush is a yeast infection, also called Candida or Candidiasis. But although thrush should actually only pertain to oral yeast infection, it is used a lot nowadays to describe a vaginal yeast infection too. So I’ve used it in that context here. And, although oral thrush can also appear in young babies, I’ve limited myself to thrush in adults only.

Let’s quickly go over the cause of thrush (yeast infection) in adults. It’s mostly caused, or at least the symptoms are caused, by a yeast-like fungi called Candida Albicans which you can find in all of our bodies quite naturally. Thrush appears when the fungi overgrow and spread.

The underlying conditions that allow this overgrowth are things such as; a lowered immune system, poor diet, too many antibiotics, stress, hormonal imbalance, and some drug usage. When one or more of these conditions are in existence then the fungi can overgrow, causing thrush symptoms.

Your normal treatment is through prescription or over-the-counter medications such as creams, lotions, foams, sprays, oral suspensions, etc., depending on the location of the thrush infection. These can take some time to work, but they can eliminate the symptoms.

But, many adults cannot use them because of some nasty side effects. And, they tend just to address the local thrush symptoms not the root cause(s) as described above. The outcome can be nasty recurring thrush infections.

So more and more adults with thrush are discovering the benefits of using natural home remedies. Here are 3 home remedies for thrush in adults that you can try:

(a) Raw Apple Cider Vinegar

This must be un-distilled, raw apple cider vinegar, with no additives and has the sediment still in the bottom. This type works by adjusting body pH which can help to prevent further fungal growth.

Add 3 teaspoons to a large glass of water and stir well. Drink a glass 3 times a day. You can douche by mixing 2 tablespoons in 2 quarts of warm water. Alternatively you can add 2 cups of apple cider vinegar into a low, warm bath and bathe for about 20 minutes or so.

(b) Fresh Garlic

Fresh garlic has fantastic antifungal benefits. Eat garlic every day. Good garlic capsules if you don’t like the odour on your breath. Pulp it into a smooth paste and coat the affected area. For inside the vagina wrap muslin around a peeled clove and leave in overnight.

(c) Natural Yogurt

Natural yogurt with no added sugar, no fruit and no other additives contains Lactobacillus acidophilus which are live beneficial bacteria that can attack the Candida fungi. So eat every day. You can also coat it over the localized area. And for inside the vagina, just coat a regular tampon and leave in overnight.

Now, whilst these 3 natural remedies for thrush in adults can be effective, they probably aren’t enough to actually cure your thrush on their own. Remember the underlying conditions above? These have to be addressed if you are to be confident that it’s not just the symptoms of thrush that have gone, but that the root cause has also been taken care of as well.

In this way you can be better assured that your thrush won’t keep returning (recurring thrush) and causing you serious health problems down the road. See below…

The Relationship Between Hepatitis and Oral Health

Hepatitis, more particularly Hepatitis C, has been associated with the decline or worsening of the oral health condition of patients infected with the diseases. As such, these patients experience problems not just pertaining to the health of their teeth and mouth, but also with their quality of life as manifested by their reluctance to interact with other people in society due to their very poor oral health.

Before we further discuss the state of the oral health of people with hepatitis, let us first understand what hepatitis is especially hepatitis C.

Hepatitis is the overall term used to describe an inflammation or infection of the liver. The most common variation of this is the hepatitis C. Hepatitis C is caused by a virus (HCV or Hepatitis C Virus) that infects the liver.

A large number of people may not be aware that they are infected with the hepatitis C virus mainly perhaps because of the lack of symptoms and also due to a mild infection. The problem with this is that it may take years before the symptoms start to show in which case it means the liver is already heavily infected and perhaps even damaged.

There are various causes of hepatitis C, ways in which a person can get the infection. The following are the most common means:

1. Most hepatitis C infections are caused by infected needles. The ones with the most probability of infection are from needles used in administering illegal drugs and also needles used for tattooing.

2. Blood transfusion is also a probable cause but this has become rarer especially since 1992 when tests were finally developed to indicate hepatitis C infection in donor blood.

3. Other probable causes are through sexual intercourse and a pregnant mother with hepatitis C transferring the infection to her unborn child. These last two are less common than from blood transfusions and needles.

Now in relation between hepatitis C and oral health of infected patients, these people are more prone to having tooth decay and other tooth abnormalities. And in a society wherein the aesthetics of any body part is highly regarded, having an unattractive smile due to poor teeth has caused great loss of self-esteem to hepatitis C patients. They are generally uncomfortable with their appearance and thus they prefer not to interact with other people especially with strangers. The other related emotional impact can just be easily surmised.

The most common oral health complaints of these patients are toothache, chronic pain in the mouth especially with the gums and difficulty relaxing due to the pain.

Hepatitis C patients always have higher risks for poor oral health. They are more likely to develop tooth decay, periodontal diseases, sensitive teeth, soreness of the mouth and the gums and bleeding. They also will likely suffer from having what is referred to as salivary gland dysfunction which is a reduction in the volume of the saliva. With less saliva, patients can suffer from halitosis or bad breath and frequent dryness of the mouth. An estimated 80% of hepatitis C patients are expected to incur this salivary gland dysfunction.

Cirrhosis Diet – You Must Read About These 3 Key Herbal Medicines

A cirrhosis diet is about more than just the kinds of foods you eat or don’t eat.Now, your doctor probably already has you taking some medications, but those really only treat the symptoms. That’s why the following three herbal medicines are so important to understand. Because they actually treat the cause, and not just the symptoms.

1. Gotu Kola: This herbal medication increases energy, is a blood cleanser, helps one cope with stress and prevents and reverses internal scarring, which is basically how liver cirrhosis starts.

2. Globe Artichoke: This one prevents vomiting, lowers cholesterol and protects and restores the liver. It’s a great remedy to treat hepatitis, and therefore is a great herb to treat one of the causes of cirrhosis and help prevent it from developing.

3. St. Mary’s Thistle (also known as Milk Thistle): St. Mary’s Thistle protects the liver, is an anti-inflammatory, assists with regenerating liver cells and helps with detoxification. This is one of the most well known treatments for different liver disorders and can often extend the lifespan in people who have severe liver disease.

Again, Gotu Kola, Globe Artichoke and St. Mary’s Thistle are some great herbal medicines that should be a part of your cirrhosis diet plan. But please, talk to your doctor and make sure these fit in with the medications that you’re already taking.

It’s good to explore alternative treatments, but you want to ensure you’re not overriding something else your doctor is prescribing.

Also note that this is only a small piece of the cirrhosis diet puzzle. The good news is that all the pieces of the puzzle have already been put into place. All you have to do is click the link. Get your liver and your life back.

Different Methods Of Kidney Stone Treatment

Kidney stones (also known as renal calculi) are a common but notoriously painful condition. Kidney stone treatment may be accomplished in several different ways, ranging from the stones passing through the system without any aid to open surgery. It is possible for kidney stones to dissolve, but this is very rare. Some of the most important factors that physicians consider are both the size of the stone and its location.

Some doctors and patients simply opt to do nothing at all. If the kidney stones are small they may pass easily without treatment. A physician might suggest increasing water intake. Pain medication may be prescribed to alleviate some of the discomfort. Another reason that this plan (or lack thereof) would be a viable option is if the stones are not causing any pain, infection, or blockage.

Lithotripsy (or extracorporeal shock wave lithotripsy) is a kidney stone treatment that uses powerful sound waves to penetrate through the body and break up the stones. Usually x-rays or an ultrasound is necessary to locate the stones. Lithotripsy itself is non-invasive and painless, but sedatives or local anesthesia may be used to prevent pain while the stone fragments pass through the system. This is usually an outpatient procedure. Some stones may not fully break down, and may require additional treatment in the future.

During an endoscopic treatment a device with a small camera, called an endoscope, is inserted into the bladder, and this serves as a guide for the physician to assess the location and size of the stones. The endoscope can be moved through the bladder, urethra, and even as far as the kidneys themselves. If the size of the stone is deemed suitable, laser treatment may be used to break the stone into fragments or the entire stone may be removed with the scope.

Another kidney stone treatment option is called a percutaneous nephrolithotomy. This procedure is usually not the preferred method of treatment because a full recovery may require one to two weeks, but it is generally successful for removing stones that are located within the kidneys. The doctor must make an incision near the site of the stone. A hollow tube and probe combination is inserted into the kidney. The stones are then removed through the tube.

Open surgery is rarely utilized to remove the stones, often only if all other methods have failed. A surgeon will make an incision to directly remove the stones from the kidneys. A catheter is inserted to drain urine for the kidney until it heals.

Prevention is perhaps the best type of treatment for future kidney stones, because recurrences aren’t uncommon. Drinking plenty of water, making healthy changes in food choices, or some types of medication may aid in preventing these stones.

Lead poisoning and the gout connection

Recently, gout has inundated the business and health news. The big stories are about US Federal Drug Administration’s approvals of new uric acid lowering drugs for gout and hyperuricemia. Scientists at John Hopkins University also made the news claiming to have found the “gout gene.”

Population studies indicate that there is an alarming worldwide increase of gout, and the pharmaceutical companies see a potential billion-dollar a year market in developing new uric acid lowering drugs. The rising tide of gout suffers has also sparked new interest among financially stressed universities as a means to obtain lucrative research grants.

Uric acid is a product of the liver and is essential to many metabolic functions, such as regulating protein synthesis, forming the DNA, and regulating body temperature as well as functioning as a metabolic antioxidant and eliminating wastes from the body.

When kidney function is somehow impaired and does not eliminate uric acid properly, the result is a buildup in the blood (hyperuricemia). In some people that causes painful gout.

Today, most gout research is predicated on archaic notions and misinformation about the causes of gout. Consequently, many gout drugs simply alleviate a symptom and mask potentially fatal health problems.

The foremost misconception is that the primary cause of gout is overindulgence of rich foods and alcohol consumption. This misconception takes its roots from face value accounts of the indulgent lifestyles associated with gout suffers of historical significance.

Many researchers use that erroneous assumption as a factual foundation for scientific research into formulating new drug treatments for gout. However, throughout history there is an inextricable link between lead poisoning and gout (saturnine gout) among the aristocracy and affluent. Most researchers and medical professionals either ignore or are ignorant of the historic lead poisoning/gout connection. 

The cause of gout among the celebrities of ‘olde’ wasn’t so much about what they ate and drank, but more related to the lead content of what they ate from, what foods and drink were stored in, lead acetate sweetening agents, use of lead based cosmetics, paints and pigments, and even the use of lead salts in the medicines.

The prominent figures in history always put forth as examples of gout suffers were almost certainly afflicted with lead poisoning that caused their gout.

Lead poisoning promotes kidney damage and inhibits uric acid excretion causing it to buildup in the blood (hyperuricemia). Hyperuricemia is the most common cause of gout, and toxicologists view gout as a primary symptom of lead poisoning.

Benjamin Franklin is an example of a famous person often cited in gout articles mainly because he was a rotund individual known for his enjoyment of the good life, and perceived overindulgent lifestyle.

In Franklin’s day, lead poisoning was of epidemic proportions on both sides of the Atlantic. During his lifetime, there was extensive use of lead products to make food storage containers, glass, and glazes for pottery. Lead acetate was a primary sweetener for bread, desserts, wines, and food. They painted their homes with lead based paints, and it was in the distilled spirits and fortified wines they drank as well as the containers in which they were stored. They added lead to tobacco snuff and even to black pepper. Hair and bone analysis of exhumed skeletal human remains from the American Colonial Period commonly show high levels of lead.

In the 18th – 19th centuries, there was also gout epidemic in Britain attributed to the consumption of lead acetate laced fortified wines and cider made by lead presses (Devon Colic). It was also commonplace for the affluent gentry and aristocracy of that period to have a bowl of lead acetate sitting on the dinner table for those who desired added sweetness to their food or drink.

Gout was also rampant among the patricians and plebeians of the Roman Empire, as was lead poisoning. Historians view lead poisoning as a primary factor in the fall of the Roman Empire. The documented relationship between lead poisoning and gout dates back to the early Egyptians. Analysis showed high lead levels in the mummies’ hair and there was also documentation of gout among the royalty.

Down through 6000 years of documented history, the association between lead poisoning and gout with historical figures is unequivocal.

In the modern annals of toxicology and history of lead poisoning, the gout of ‘olde’ is always attributed to lead poisoning, not the overindulgence of protein rich foods and alcohol as most medical professionals state as fact.

Today, the increasing incidence of gout in populations and the time-line for developing gout symptoms can once again be associated with lead poisoning. This is due to the extensive use of leaded petrol, lead-based paint, and industrial pollution in the post World War II era.

People born between 1945 and 1971 stand the greatest chances of developing gout and hyperuricemia as symptoms of lead poisoning. Aside from all other exposures to lead, the most ubiquitous during that period was from the use of leaded petrol.

From the onset of adding lead to petrol, many scientists foresaw the potential of mass subclinical lead poisoning among populations.

In 1924, Yandell Anderson, professor of applied physiology at Yale University, the inventor of the gas mask, was among those who warned about mass poisoning from leaded petrol.

In 1965 that Clair Patterson, a geochemist, proved that lead in human bodies had increased 100 times since the introduction of lead in petrol.

In 1980, the US National Academy of Sciences said that leaded petrol was the greatest source of atmospheric lead pollution.

Leaded petrol was most likely the worst culprit aside from lead-based paints and lead plumbing in homes for lead poisoning. Not only did the lead from petrol pollute the air, soil, and water, but also the food crops used to feed people and farm animals. Lead pollution from petrol became a part of the food chain, and was in everything we consumed.

The most insidious aspect of the pollution from leaded petrol is that it can readily be absorbed through the skin and directly into the blood stream. The pollution also has the mischievous distinction of being readily available via all routes of exposure: oral, inhalation, and absorption through the skin.

With the phasing out of leaded petrol in the United States, the blood lead levels of all Americans declined 78 percent between 1978 and 1991. The decline was in exact proportion to the declining levels of lead in the petrol supply and coincided with the reduction of lead air pollution. The results were similar in countries around the world that phased out the use of leaded petrol for on-road vehicles.

However, just because there was dramatic reduction of environmental pollution from leaded petrol, the health problems associated with long-term exposure were not. The adverse health effects of lead poisoning are not always immediate and often manifest themselves decades later in the form of hypertension, cardiovascular disease, presenile dementia, impaired cognitive ability, and kidney damage, among others, including gout.

95% of all lead to which we are exposed is stored in the bone, and has a half-life of 28 years.

Lead is what toxicologists refer to as a “bone seeker.” It acts like calcium and becomes part of the bone structure. Consequently, our bones are a lead repository, and due to low-level, environmental lead exposures over a period of years, the lead content can reach toxic levels.

Recently, researchers found convincing evidence that many gout cases may well be associated with reabsorption into the blood of ambient lead stored in our bones.

The reason for their conclusions is that a process called bone remodeling becomes more active in middle-aged people and increases with ageing.

Bone remodeling occurs when the bone releases calcium part of the natural calcium turnover in the body. The metabolic process also releases the stored lead that causes kidney damage which in turn inhibits uric acid excretion. There is a subsequent buildup of uric acid in the blood (hyperuricemia) that causes gout in some people.

According to some research, lead reabsorption from bone remodeling may be a primary cause of hyperuricemia and gout among middle aged and elderly men, as well as postmenopausal women.

The result of reabsorbed bone-lead is lead poisoning in people not otherwise exposed to occupational levels during their lifetime. In U.S. population surveys, the results showed that second only to young children, older adults have among the highest blood lead levels from non-occupational exposures.

While exposures to the average person may be below occupational levels, over time these little exposures can add up to toxic levels in the bones. The actual impact of subchronic lead poisoning on an individual’s health does not manifest until bone remodeling begins to increase with age and larger amounts of stored lead enter the blood stream.

Reliance on the results of simple blood tests for lead levels is a poor indicator of the total body burden, and only reflects recent exposures. X-ray fluorescence is the standard for accurate determination of the total body burden.

Because of the unequivocal, historic association between lead poisoning and gout and the more recent reality of population scale exposure to lead pollution from leaded petrol, subclinical lead poisoning should be the first thing a doctor considers as the primary cause of gout.

Prescribing uric acid lowering drugs will do little more that mask the problem. If a patient is suffering from lead poisoning, at the end of the day, the doctor may lower the uric acid levels, temporarily relieving the gout attacks with drugs. However, the patent is still suffering from the deleterious effects of lead poisoning and the kidneys continue deteriorating – the doctor has only treated a symptom, not the cause.

When it comes to treatment, toxicologists should address lead related gout intervention, not medical doctors. A toxicologist would most likely recommend chelation therapy and therapeutic doses of vitamin C. Therapeutic dosages of vitamin C and potassium acetate/citrate also facilitate the excretion of uric acid without further damaging the kidneys with uric acid lowering drugs that only address the symptom.


Duodenal Ulcer Information

The symptoms of duodenal ulcers include heartburn, stomach pain relieved by eating or taking antacids, weight gain, and a burning sensation at the back of the throat. The patient is most likely to feel discomfort two to four hours after meals, or after having citrus juice, coffee, or aspirin. About fifty percent of patients with duodenal ulcers awake during the night with pain, usually between midnight and three a.m. If an ulcer is bleeding, the patient may have vomit containing bright red blood or digested blood that looks like brown coffee grounds and black, tarry bowel movements.

Stomach is called a gastric ulcer; of the duodenum, a duodenal ulcer; and of the esophagus, an esophageal ulcer. An ulcer occurs when the lining of these organs is corroded by the acidic digestive juices which are secreted by the stomach cells. Peptic ulcer disease is common, affecting millions of Americans yearly. The medical cost of treating peptic ulcer and its complications runs in the billions of dollars annually. Recent medical advances have increased our understanding of ulcer formation. Improved and expanded treatment options are now available.

A peptic ulcer is erosion in the lining of the stomach or duodenum (the first part of the small intestine). The word “peptic” refers to pepsin, a stomach enzyme that breaks down proteins. If a peptic ulcer is located in the stomach it is called a gastric ulcer. Small ulcers may not cause any symptoms. Large ulcers can cause serious bleeding. Most ulcers occur in the first layer of the inner lining. A hole that goes all the way through is called a perforation of the intestinal lining. A perforation is a medical emergency.

Duodenal ulcers usually occur in younger people, while gastric ulcers occur in older age groups. It is still not clear what, if any, role stress plays in the development of ulcers. Alcohol and diet are not felt to play a very important role in the formation of ulcers. Some ulcers are caused by an organism called Helicobacter pylori, some are due to medications, and a few are caused by stomach or intestinal cancer. Therefore, treatment and long-term outcome depends on the cause of the ulcer.

The understanding of the etiology of duodenal ulcer has changed dramatically in the latter part of the 20th century. Historically, duodenal ulcer was thought to be a disease related to diet and environmental stress alone. Subsequent studies revealed the importance of pepsin and acid secretion in the pathogenesis of duodenal ulcer. The most revolutionary change in the knowledge of duodenal ulcer was the discovery in 1982 that the bacterium H pylori was present in most patients.

The most common symptom of a duodenum is a gnawing or burning pain in the abdomen between the breastbone and navel. Duodenal ulcers typically cause symptoms 2 to 5 hours after meals, when the stomach is empty, and can be relieved by eating. Gastric ulcers, on the other hand, are classically made worse by eating. You may experience pain soon after meals, and food won’t improve symptoms. For each, the duration of pain can be from a few minutes to a few hours.

If a person does not receive treatment for ulcers, it could lead to a bleeding ulcer (the ulcer has eaten into blood vessels and the blood has seeped into the digestive tract), a perforated ulcer (the ulcer has eaten a hole in the wall of the stomach or duodenum and bacteria and partially digested food has spilled into the hole, causing inflammation) or a narrowing and obstruction of the intestinal opening preventing food from leaving the stomach and entering the small intestine.

Altaflora Remedies for Indigestion Which Provide Symptom Relief Without Any Side Effects

If one has a digestive problem and there is no acidity involved, it is useless to treat oneself with an anti-acid, as there is no need to suppress acidity.

There are a number of natural ingredients which provide relief from digestive problems by treating the underlying causes.

Digestive enzymes, like Bromelain and Papaya provide relief by helping digestion when the underlying cause is delayed gastric emptying. Bromelain is derived from the pineapple fruit and is a lipolytic enzyme (an enzyme capable of digesting fat globules). Papaya is an enzyme which helps reduce gas, bloating, and fullness after a high-fat meal.

Artichoke has a choleretic (bile stimulating) action, and helps bile flow to increase significantly. Artichoke is an ideal treatment for mild indigestion—particularly following a meal high in fat. It also helps to reduce nausea, abdominal pain, constipation, and flatulence.

Licorice is a natural acid-blocker. It is also used as a complimentary treatment to H2 antagonists and proton pump inhibitors when treating gastro esophageal reflux (GERD) disease which is a disorder of the esophagus that causes frequent symptoms of heartburn.

Aloe Vera is a remedy to indigestion and nausea caused by overeating, wrong food choices or combinations, stress and stomach bugs. An Aloe layer is formed over the food being digested and this gives a soothing effect.

Calendula has soothing effects and has been used for the natural relief of stomach ulcers and inflammation.

Peppermint Oil is classified as a carminative and is excellent when the underlying cause of indigestion is a hypo motility – a substance that prevents and relieves intestinal gas.  It may also relieve spasms in the intestinal tract. Peppermint oil or peppermint tea is often used to treat gas and indigestion.

What would be better than having all these advantageous substances combined into one product which can be bought over the counter?

Altaflora Gastrogel Syrup, by Alta Care Laboratoires – Paris is a 100% natural supplement containing all the above mentioned digestive enzymes, extracts and essential oils. It is a unique formulation of certified concentrated aloe, essential oils and digestive enzymes, combined with herbs recognized for their soothing and digestive properties.

Altaflora Gastrogel has the advantage of being manufactured in syrup form. Thus the ingredients used in Altaflora Gastrogel Syrup are fresh and not processed, unlike the case of tablets, where the efficacy of the ingredients is lessened, due to manufacturing processes like drying or compressing in which the ingredients lose some of their activity and some of their properties are lost or altered.

Since tablets or capsules take longer to digest than syrup, Altaflora Gastrogel guarantees faster and immediate symptom relief.

Alta Care Laboratoires – Paris, do not dilute their syrups with water, thus the active ingredients are stronger and therefore give better effective results. The ingredients of Altaflora Gastrogel Syrup are diluted in sugar-free honey and Pineapple juice, guaranteeing an excellent taste!

If you suffer from common digestive problems Altaflora Gastrogel is definitely worth a try to treat the underlying cause of indigestion! Take one tablespoon of Altaflora Gastrogel Syrup after meals or when symptoms appear. 

Altaflora Gastrogel Syrup is available in 200ml or in the maxi size 500ml bottles and can be purchased from pharmacies.

Remedies of Food Poisoning

Sometimes eating the wrong foods causes constipation. Increase your fiber intake. Take psyllium husks. Be sure to drink lots of water when you use fiber supplements. Eat more raw vegetables and fruit. Prunes and figs are laxatives. And don’t forget the old standby beans.

Oftentimes, it does happen to be the foods you are eating that are giving you a tummy ache. In this case, the best solution is to drink a good tea that will help settle your stomach and aid in digestion. A simple green tea or just a cup of strong black tea is good as is tea made from chamomile, ginger, mint or cinnamon.

Food Poisoning is caused by eating something that does not agree with your stomach. Harmful bacteria or viruses may have been eaten. You may also feel dehydrated, accompanied by diarrhea and vomiting. Eating tainted food or drinking water may cause food poisoning.

Over eating generally happens in the evening approximately 2 hours after eating. This may be accompanied by nausea or vomiting. This indigestion is typically caused by eating rich or fatty foods.

Some new remedies like Botox, the well known wrinkle treatment can also be an answer to this problem. Though made from the toxin which causes food poisoning, this toxin can be effective in deactivating the sweat glands for some time providing a temporary relief of sweating in problem areas.

One type of food poisoning that is rare but often times fatal is called botulism. Most of the times this is caused by a bacteria that is formed when foods are improperly canned.

The foods that most commonly develop this are foods that are low in acid content like beans and corn. What happens is a bacteria that doesn’t get killed in the canning process develops and grows inside the jar which produces a toxin.

The seed’s extract is extra bitter, so use tablets or capsules instead of the liquid, and take three times a day. If you do use the liquid, use five drops in a glass of water. Another helpful product to carry with you is activated charcoal which is explained in more detail below.

Food Poisoning is caused by eating something that does not agree with your stomach. Harmful bacteria or viruses may have been eaten. You may also feel dehydrated, accompanied by diarrhea and vomiting. Eating tainted food or drinking water may cause food poisoning.

Hyperacidity is the condition that is caused by too much acid in the stomach. This can be caused by too much alcohol consumption, overeating, and generally unhealthy meal. Various types of acidity foods may also cause hyperacidity.

Food poisoning is one of the most uncomfortable illnesses that one can develop. This disease, which typically only lasts for 24 to 48 hours, causes severe digestive system discomfort in its victims. People can get food poisoning through the ingestion of contaminated foods or by coming into contact with someone else that has been infected.

You become infected with food poisoning when you eat food that has been contaminated by an attacking microorganism. Certain strands of bacteria, viruses, and even parasites may cause this illness. These dangerous microbes, often found in animal feces, may come into contact with and infect food during just about any stage of packaging and processing.

Food poisoning, an illness not typically thought of as a life-threatening condition, can make its victims quite miserable for the few days it affects them. Those who suffer from this condition will experience extreme abdominal cramping, nausea and vomiting, and persistent diarrhea.

Signs of food poisoning may range from mild to life threatening. Vomiting, fever, diarrhea, nausea, cramping are all signs of poisoning. Remember you many suffer from only a few of the symptoms or all of the symptoms. Generally symptoms come on withing 48 hours after eating or drinking the contaminated foods/drinks.

If you are experiencing mild diarrhea or vomiting then you can probably self treat at home. On the other hand if you are suffering from food poisoning and already have compromised heath, if you are pregnant, dehydrated or if you don’t seem to be getting any better after a day or so then seek medical treatment.

The good news is that, if the gum disease is detected on its early stage, it can be treated and reversed. There are lots and lots of natural gum disease remedies readily available. Using natural gum disease remedies will not only give fast healing process, it will also provide better oral health care.

Eating a banana each day works like an antacid to soothe
heartburn. If you’re already stricken with indigestion, eating
pineapple or papaya (or drinking the juice) can help settle your
stomach naturally. Some people also claim that eating a teaspoon

Home Remedies For Gas In The Stomach

Gas can be not only uncomfortable, but embarrassing as well. You will be happy to know that not only are there simple steps that you can take to avoid the problems, there are several home remedies for stomach gas treatment once the problem has arisen.

Initially, many gas issues can be avoided by changes in the diet. Gas producing foods—such as cabbage, Brussels sprouts, cauliflower, broccoli and beans—can simply be avoided. In the alternative, adding a digestive aid to the food can help prevent gas from developing when the offending food is eaten. Substituting tofu for beans is another way to still keep the protein intake high but substitute a more digestible protein. Avoiding artificial sweeteners, especially sugar alcohols, will greatly reduce gas production and its associated stomach cramping. Cutting out carbonated beverages will go a long way to reducing gas in the stomach as well.

Another notorious gas producing food is milk and milk products. In the adult population, lactose intolerance can manifest as gas production. Some of the sufferers of lactose intolerance produce copious amounts of gas, hard for both the sufferer and for those around them. Avoidance is really the only way to avoid the painful combination of dairy and lactose intolerance.

But the simplest thing that can be done in the home to improve stomach gas is to chew your food slowly and completely. Gas in the stomach is, in large part, air. The aromatic portions of the gas in the stomach are made of chemicals like esters. While pungent, they are really a small fraction of the gas produced. Anything that will reduce air intake into the gut is a good first step to the overall reduction of gas.

Once you have a case of stomach gas, there are home remedies for stomach gas that will ease the pain. The herbs anise, peppermint, chamomile, or fennel can be made into a soothing tea that is very helpful. Avoid all types of tobacco products and increase the amount of fluid that you are drinking, especially water. In extreme cases, try lying on your back and drawing your knees up to your chest. It is easier to expel painful gas that way.

Other herbal and home remedies for stomach gas include a tea made from blanched verbena leaves. One teaspoon of fresh ginger and I teaspoon of lime juice taken together will relieve stomach pain due to gas. Parsley tea is another herbal remedy that can be used as a home remedy for stomach gas. Tea made from passion fruit and peach leaves is also said to cure gas attacks.

Lymphedema Therapy – How to Finally Get Some Relief From Your Pain

Lymphedema is caused when damage is done to the lymph vessels or nodes, and can develop after surgery or the formation of scar tissue, and in rare cases is caused by abnormalities in the lymph vessels at birth. If you’re one of the people suffering from the effects of lymphedema, such as the buildup of lymph fluids in the body, then you’re probably weighing your therapy options on the best treatment for it. Compression, massage, and a lymphedema pump, are all different types of lymphedema therapy that people are using to help get relief.

Compression on the affected areas of the body is a very common method of lymphedema therapy. It’s a very common route because it is a simple, easier, and less costly than other methods. Compression involves wrapping bandages around the affected areas of the body. Where the lymph vessels are affected, several layers of gauzing are put underneath a low-stretch bandage. The bandage provides mild pressure on the area, and keeps swelling and skin hardening down.

Massage can be used in accord with other methods of therapy. A massage therapist that specializes in lymphedema treatment is great because they have been specially trained to do the massage correctly. The massage therapist will help promote the flow of the lymph from the affected areas through other vessels in the body. Massage therapy is great to use in tandem with the bandaging, because it doesn’t hinder the effectiveness of the bandages, and is a non-invasive way to get relief from the symptoms.

The lymphedema pump is another method utilized by people who may have trouble getting to a massage therapist for treatment. The pump works by simulating the way the lymph would be pushed out of affected areas, and increases the flow of the fluid to the circulatory system. The pump, as with the massage, is very useful when added to a compression or wrapping therapy, because it can either be done in the home or done at a clinic or other professional setting.

If you are suffering from lymphedema, there are many ways for you to get relief from the swelling and infections. People choose many different types of therapy, sometimes choosing to do several at a time. It’s best to consult with a doctor about what you can begin doing, and the proper ways to begin therapy. Depending on the severity of it, you may pick and choose between other methods of lymphedema therapy. Your doctor should be able to provide you with information about how much therapy and treatment you would need in order to return to your old self.

An Ultrasound Test Is High Frequency Sound

An ultrasound test is a radiology technique, which uses high- frequency sound waves to produce images of the organs and structures of the body. The sound waves are sent through body tissues with a device called a transducer. The transducer is placed directly on top of the skin, which has a gel applied to the surface. The sound waves that are sent by the transducer through the body are then reflected by internal structures as “echoes.” These echoes return to the transducer and are transmitted electrically onto a viewing monitor. The echo images are then recorded on a plane film and can also be recorded on videotape. After the ultrasound, the gel is easily wiped off.

The technical term for ultrasound testing and recording is “sonography.” Ultrasound testing is painless and harmless. Ultrasound tests involve no radiation and studies have not revealed any adverse effects.

For what purposes are ultrasounds performed?

Ultrasound examinations can be used in various areas of the body for a variety of purposes. These purposes include examination of the chest, abdomen, blood vessels (such as to detect blood clots in leg veins) and the evaluation of pregnancy. In the chest, ultrasound can be used to obtain detailed images of the size and function of the heart. Ultrasound can detect abnormalities of the heart valves, such as mitral valve prolapse, aortic stenosis, and infection (endocarditis). Ultrasound is commonly used to guide fluid withdrawal (aspiration) from the chest, lungs, or around the heart. Ultrasound is also commonly used to examine internal structures of the abdomen. Gallstones in the gallbladder are easily detected, as are kidney stones. The size and structure of the kidneys, the ureters, liver, spleen, pancreas, and aorta within the abdomen can be examined. Ultrasound can detect fluid, cysts, tumors or abscess in the abdomen or liver. Impaired blood flow from clots or arteriosclerosis in the legs can be detected by ultrasound. Aneurysms of the aorta can also be seen. Ultrasound is also commonly used to evaluate the structure of the thyroid gland in the neck.

During pregnancy, an ultrasound can be used to evaluate the size, gender, movement, and position of the growing baby. The baby’s heart is usually visible early, and as the baby ages, body motion becomes more apparent. The baby can often be visualized by the mother during the ultrasound, and the gender of the baby is sometimes detectable.

How do patients prepare for an ultrasound?

Preparation for ultrasound is minimal. Generally, if internal organs such as the gallbladder are to be examined, patients are requested to avoid eating and drinking with the exception of water for six to eight hours prior to the examination. This is because food causes gallbladder contraction, minimizing the size, which would be visible during the ultrasound. In preparation for examination of the baby and womb during pregnancy, it is recommended that mothers drink at least four to six glasses of water approximately one to two hours prior to the examination for the purpose of filling the bladder. The extra fluid in the bladder moves air-filled bowel loops away from the womb so that the baby and womb are more visible during the ultrasound test.

How are results transmitted to the patient and doctor?

The ultrasound is generally performed by a technician. The technician will notice preliminary structures and may point out several of these structures during the examination. The official reading of the ultrasound is given by a radiologist, a physician who is an expert at interpreting ultrasound images. The radiologist records the interpretation and transmits it to the practitioner requesting the test. Occasionally, during the ultrasound test the radiologist will ask questions of the patient and/or perform an examination in order to further define the purpose for which the test is ordered or to clarify preliminary findings. Plain x-rays might be ordered to further evaluate early findings. A summary of results of all of the above is reported to the practitioner who requested the ultrasound. They then are discussed with the patient in the context of overall health status.

The effect of thrombolytric drugs on cardiac enzymes, Creatine Phospho kinase and Creatine Kinase -MB, in myocardial Infarction”

“The effect of thrombolytric drugs on cardiac enzymes, Creatine Phospho kinase and Creatine Kinase -MB, in myocardial Infarction”.


Myocardial infarction refers to a dynamic process by which one or more regions of the heart muscle experience a severe and prolonged decrease in oxygen supply because of insufficient coronary blood of subsequently, necrosis or death to the myocardial tissue occurs.

The onset of the myocardial infarction process may be sudden or gradual and the progression of the event to complete takes approximately 3 to 6 hours.


Myocardial infarction is the leading cause of death in the United States (US) as well as in most industrialized nations throughout the world. Approximately 800,000 people in the US are affected and in spite of a better awareness of presenting symptoms, 250,000 die prior to presentation to a hospital.4 The survival rate for US patients hospitalized with MI is approximately 90% to 95%. This represents a significant improvement in survival and is related to improvements in emergency medical response and treatment strategies.

In general, MI can occur at any age, but its incidence rises with age. The actual incidence is dependent upon predisposing risk factors for atherosclerosis, which are discussed below. Approximately 50% of all MI’s in the US occur in people younger than 65 years of age. However, in the future, as demographics shift and the mean age of the population increases, a larger percentage of patients presenting with MI will be older than 65 years.

Men are more susceptible than women, but the risk is more in female than in male after menopause.


The coronary arteries supply the capillaries of the myocardium with blood

The right coronary artery (RCA) supplies the right atrium and ventricle, the inferior portion of the left ventricle, the posterior septal wall and the SA and AV nodes

The left coronary artery (LCA) consists of two major branchiate left anterior descending (LAD) and the circumflex (LCX).

The LAD artery supplies below the anterior wall of the left ventricle, anterior ventricular septum and the apex of the left ventricle.

The LCX artery supplies blood to the lateral and posterior surfaces of the left ventricle. 


Levels of cardiac markers rise overtime. Hence, enzymes are drawn in a serial pattern usually on admission and over 6-24 hrs until 3 samples are obtained.

 Enzymes commonly evaluated include CK, CKMB, LDH, TroponinT & I.

 CK-MB ratio indicates the extent of damage of the cardiac muscle. The more the ratio, the more the damage of the cardiac muscle. Troponins are  preferred markers of myocardial injury or they are very cardiac specific & are thought to rise before permanent injury develops.

Increased troponin concentrations should not be used by  themselves to rule out a heart  attack. Troponin will remain high for 1–2 weeks following MI allowing easy diagnosis if patient presents late with an old MI as other CE’s will not be raised unless reinfarction occurs.

Elevation of Cardiac Enzymes in Myocardial Infarction

Enzyme         Rises in        Peaks in      Normalizes in    Normal Value    CKMB ratio

CK                 12 hrs          16-30hrs      3-5 days            35-232IU/L

CKMB            4-8 hrs         24 hrs           72 hrs                < 51IU/L           <6% 

Troponin I    3-6 hrs         20 hrs           14 days              0.0-0.4 ng/ml 

Troponin T    2-4 hrs         8-12 hrs       14 days              0.0-0.1 ng/ml

LDH              12 hrs          12-24 hrs     10 days             100-190 IU/L


The most common sites of MI are in the left ventricle, the chamber of heart which has the greatest work load. Tissue changes that occur in the myocardium are related to the extent to which the cells have been deprived of oxygen. Total deprivation results in an area of infarction in which the cells die and the tissue become necrotic.

Necrosis in this area is evident with in 5 to 6 hours after the occlusion. In response to this necrosis the body increases its products of leukocytes, which aid in the removal of dead cells. As collateral circulation enlarges, it brings fibroblasts, which form a connective tissue scar with in the area of infarction. Usually, the formation of fibrous scar tissue is complete with in 2 to 3 months.

Immediately surrounding the area of infarction is a less seriously damaged area of injury. It may deteriorate and thus extend the area of infarction or with adequate collateral circulation; it may regain its function with in 2 weeks.

The outer most area of damage is the zone of ischemia which borders the area of injury. The cells in this area are weakened by decreased oxygen supply, but function can return usually with in 2 to 3 weeks after the onset of occlusion.


There are two types of risk factors for heart attack, including

  1. Inherited factors
  2. Acquired factors

Inherited factors

These are risk factors you are born with that cannot be changed, but can be improved with medical management and life style changes. Following are most at risk-

  • persons with inherited hypertension
  • persons with inherited low levels of HDL or high levels of LDL
  • persons with a family history of heart disease aging men and women
  • persons with diabetes mellitus [ type 1 diabetes ]
  • women, after the onset of menopause- generally, men are at risk, at an earlier age than women, but after the onset women are equally at risk

Acquired factors

These are risk factors that are caused by activities that we choose to include in our lives that can be managed through life style changes and clinical care. Following are most at risk-

  • Persons with acquired hypertension
  • persons with acquired low level of HDL or high level of LDL
  • cigarette smokers
  • people who are under a lot of stress
  • individual who lives a sedentary life
  • persons overweight by 30 % or more


1.      Different degrees of damage occurs to the heart muscle-

Zone of necrosis: death to the heart muscle caused by extensive and complete oxygen deprivation that is, irreversible damage

Zone of injury: region of heart muscle surrounding the area of necrosis; inflamed and injured, but still viable if adequate oxygen can be restored.

Zone of ischemia: region of the heart muscle surrounding the area of injury, which is ischemic and viable; not endangered unless extension of the infarction occurs.

2.      According to the layers of the heart muscle involved, MI can be classified as-

Transmural or Q wave infarction; area of necrosis occurs throughout the thickness of the heart muscle. Subendocardial or non transmural infarction; area of necrosis is confined to the innermost layer of the heart muscle.

3.      Location of the MI is identified as location of the damaged heart muscle within the left ventricle inferior, anterior, lateral and posterior-

Left ventricle is the most common and dangerous location for MI, as it is the main pumping chamber of the heart

Right ventricular infarction commonly occurs I junction with damage to the inferior and or posterior wall of the left ventricle

4.      Region of the heart muscle that becomes damaged determine by the coronary artery that becomes obstructed

Left main coronary artery

Circumflex branch

Anterior ascending branch

Great cardiac vein

Middle cardiac vein

Right cardiac vein


1)            Chest pain

  • not relieved by the rest over sublingual vasodilator therapy
  • severe steady sub sternal chest pain of a crushing and squeezing nature
  • may radiate to the arms, neck, jaw and shoulders
  • continuous more than 15 minutes
  • may produce anxiety and fear

2)            Diaphoresis

3)            Hypertension or hypotension

4)            Bradycardia or tachycardia

5)            Palpitation, severe anxiety, dyspnea

6)            Disorientation, confusion and restlessness

7)            Fainting, marked weakness

8)            Nausea, vomiting, hiccoughs

9)            Atypical symptoms such as epigastric pain abdominal distress, dull aching or tingling sensation, shortness of breath, extensive fatigue


1.      ECG changes

Generally occur within 2 – 12 hours, but may take 72 – 96 hours.

Necrotic, injured and ischemic tissue alter ventricular depolarization and repolarization

ST segment depression and T wave inversion indicate a pattern of ischemia

ST elevation indicates an injury pattern

  • Anterior small           V3 – V4 leads
  • Anterior extensive    V2 – V5 leads
  • Anteroseptal            V1- V3 leads
  • Posterior                  V1 – V2 leads, progressive R wave and ST depression
  • Anterolateral            V4 – V6, I, Avl leads
  • Apical                        V5 – V6 leads
  • Inferior                     lead ii, iii and avf [ reciprocal ]

2.      Elevation of serum enzymes and isoenzymes:

Enzymes are drawn in a serial pattern usually on admission and every 6 – 24 hours until 3 samples are obtained. Enzyme activity then is correlated to the extent of heart muscle damage

Enzymes commonly evaluated include are CK, LDH, CK-MB, AST, Troponin I, Troponin T. [Fig.4 ]

LDH 2 is normally greater than LDH 1 except when the heart muscle is damaged a reversal occurs

3.      Other findings:

White blood cell count and sedimentation rate elevates due to inflammatory process associated with damaged heart muscle.

Radionuclide imaging allows recognition of areas of decreased perfusion

Position emission tomography determines the presence of reversible heart muscle injury and irreversible or necrotic tissue, extends to which the injured heart muscle has responded to treatment also can be determined


Therapy is aimed at the protection of ischemic and injured heart tissue to preserve muscle function, reduce the infarct size, and prevent death. Innovative modalities provide early restoration of coronary blood flow , and the use of pharmacologic agents improve oxygen supply and demand, reduce and/or prevent disarrhythmias, and inhibit the progression of coronary artery disease.

1.      Opiate analgesic therapy: Morphine is used to relieve pain, improve cardiac hemodynamics by reducing preload and after load and to relieve anxiety.

Meperidine [Demerol] is useful for pain management in those patients contraindicated to morphine or sensitivity to respiratory depression.

2.      Anxiolytic agents: Benzodiazepines are used with analgesics when anxiety complicates chest pain and its relief

3.      Antiplatelet agents: Aspirin interfere with the function of the enzyme cyclooxygenase and inhibits the formation of thromboxane A2. Within minutes aspirin prevents additional platelet activation and interferes with platelet adhesion and cohesion

Other antiplatelet agents are, Clopidogrel, Ticlopidine, Dipyridamole, these agents, specifically Clopidogrel may be useful for patients who have a true allergy to aspirin and some times can be used with combination with Aspirin.

4.      Supplemental oxygen: Supplemental oxygen should be administered. The rationale for use is the assurance that erythrocytes will be saturated to maximum carrying capacity. Because MI impairs the circulatory function of the heart, oxygen extraction by the heart and by other tissue may be diminished.

5.      Nitrates: Intravenous Nitrates should be administered in MI, persistent ischemia, hypertension or large anterior wall MI. Nitrates are metabolized to nitric oxide in the vascular endothelium. Nitric oxide relaxes vascular smooth muscle and dilates the blood vessel lumen. Vasodilatation reduces both cardiac preload and after load, and decreases the myocardial oxygen requirements. Vasodilatation of the coronary arteries improves the blood flow through the partially obstructed vessels as well as through collateral vessels. When administered sublingually or intravenously, Nitroglycerin has a rapid onset of action.

6.      Beta adrenergic blocking agents: Beta blockers are recommended within 12 hours of MI symptoms and are continued indefinitely. Beta blockers decrease the rate and force of myocardial contraction and decreases overall myocardial oxygen demand. During the acute phase of MI beta blockers may be initiated intravenously

7.      Heparin: Unfractionated Heparin: intravenous unfractionated Heparin is recommended who undergo percutaneous revascularization. It is alsorecommended in patients who receive fibrinolytic therapy and non selective fibrinolytic agents such as urokinase, streptokinase and anistreplace. Heparin inhibits the additional formation and propagation of thrombi, effective when administered intravenous or subcutaneously.

Low-molecular-weight-Heparin: can be administered to MI clients not treated with fibrinolytic therapy

8.      Fibrinolytic or Thrombolytic agents: Fibrinolytic therapy is indicated with ST segment elevation. Plasminogen activators restore coronary vessels by dissolving obstructing thrombus. The plasminogen activators have been shown to restore coronary blood flow in 50% to 80% of MI patients. The successful use of fibrinolytic agents provides a definite survival benefit that is maintained for years. Reteplase has been shown to produce slightly higher 60- and 90-minute angiographic patency rates than accelerated alteplase, while adverse-event rates were equal.

However, the better early patency rate did not translate into any survival advantage at 30 days follow-up. The most critical variable in achieving successful fibrinolysis is time from symptom onset to drug administration. A fibrinolytic is most effective when the "door-to-needle" time is 30 minutes or less.

9.      Angiotensin converting enzyme inhibitors: Oral ACEI are recommended within the first 24 hours of the onset of the MI symptoms, decreases myocardial after load through vasodilatation.

10.  Anti dysarrhythmic agents: Lidocaine decreases ventricular irritability, which commonly occurs post MI.

11.  Calcium channel blockers: Improves the balance between the oxygen supply and demand by decreasing heart rate, blood pressure and dilating coronary vessels.

Diltiazem has been shown to decrease the incidence of reinfarction in patients with non-Q-Wave MIs.

12.  Percutaneous Coronary Intervention [Fig-15]: Mechanical opening of the coronary vessel can be performed during an evolving infarction. A balloon tipped catheter is introduced through a guide wire into a coronary vessel with a non calcified atheromatous lesion. The balloon of the catheter is the inflated, causing disruption of the intima and changes in the atheroma. The result is an increase in the diameter of the lumen of the coronary vessel and improvement of blood flow below the lesion.

Percutaneous coronary intervention is an alternative therapy to fibrinolysis Restoration of coronary blood flow in a MI can be accomplished mechanically by percutaneous coronary intervention (PCI). Mechanical revascularization by PCI is used as a primary therapy as an alternative to fibrinolysis when fibrinolysis is not clearly indicated or contraindicated. PCI can successfully restore coronary blood flow in 90% to 95% of MI patients.

13. Surgical Revascularization: Emergent or urgent coronary artery bypass graft surgery is warranted in the setting of failed percutaneous intervention in patients with hemodynamic instability and coronary anatomy amenable to surgical grafting. Surgical revascularization is also indicated in the setting of mechanical complications of MI such as ventricular septal defect, free wall rupture, or acute mitral regurgitation. Restoration of coronary blood flow with emergency Coronary Artery Bypass Grafting (CABG) can limit myocardial injury and cell death if it is performed within 2 or 3 hours of symptom onset. Emergency CABG carries a higher risk of perioperative morbidity (bleeding and MI extension) and mortality than elective CABG. The risk of operative mortality during emergency CABG is increased in patients, who are in cardiogenic shock, those with previous CABG surgery, and with multi-vessel disease. On the other hand, urgent CABG confers a survival benefit in patients with recurrent ischemia post-MI whose coronary anatomy is unsuitable for complete revascularization with PCI. Elective CABG improves survival in post-MI patients who have left main artery disease, three-vessel disease, or two-vessel disease that is not amenable to PCI. The timing of elective CABG post-MI is controversial, but retrospective studies indicate that when CABG is performed as early as 3 to 7 days post-MI, operative mortality is equivalent to CABG performed on non-MI patients.

14. Cardiac Stress Testing: Cardiac stress testing post-MI has established value in risk stratification and assessment of functional capacity. Stress testing is not recommended within several days post-MI. Only sub-maximal stress tests should be performed in stable patients 4 to 7 days after MI. Exercise testing identifies patients with residual ischemia for additional efforts at revascularization. Exercise testing also provides prognostic information and acts as a guide for post-MI exercise prescription and cardiac rehabilitation.

15. Lipid Management: All post-MI patients should be on an American Heart Association Step II diet (< 200 mg cholesterol/day, < 7% of total calories from saturated fats). Post-MI patients with LDL-cholesterol levels > 100 mg/dL on a Step II diet are recommended to be on drug therapy to lower LDL-cholesterol levels < 100 mg/dL. Post-MI patients with HDL-cholesterol levels < 35 mg/dL on a Step II diet are recommended to participate in a regular exercise program and on drug therapy designed to increase HDL-cholesterol levels.4 Recent data indicate the all MI patients should be on statin therapy, regardless of lipid levels or diet

16. Long-term Medications: Most oral medications instituted in the hospital at the time of MI will be continued long-term. Therapy with aspirin and beta-blockade is continued indefinitely in all patients. ACEI is continued indefinitely in patients with congestive heart failure, left ventricular dysfunction (ejection fraction < 0.40), hypertension, or diabetes. A lipid-lowering agent, specifically a statin, in addition to dietary modification is continued indefinitely 

17. Cardiac Rehabilitation: Cardiac rehabilitation provides a venue for continued education, re-enforcement of lifestyle modification, and adherence to a comprehensive prescription of therapies for recovery from MI, which includes exercise training. Participation in cardiac rehabilitation programs post-MI is associated with a decrease in subsequent cardiac morbidity and mortality. Other benefits include improvement in quality of life, functional capacity and social support. A minority of post-MI patients actually participate in formal cardiac rehabilitation programs due to either lack of structured programs, physician referrals, low patient motivation, non-compliance, or financial constraints.


Reperfusion therapy, within which we include thrombolytic therapy and percutaneous coronary intervention (PCI), which includes angioplasty and stent placement, is the greatest advance in the treatment of acute myocardial infarction

Studies have shown that many patients with AMI who are eligible for reperfusion therapy do not receive it. Moreover, of those who do receive it, the time to administration of thrombolytic therapy, or "door-to-needle time" is often delayed, jeopardizing myocardium and leading to greater morbidity and mortality.

 Clinical criteria and simple ECG parameters have limited value for the non-invasive diagnosis of myocardial reperfusion. Other methods, such as ST segment monitoring and kinetic analysis of biochemical markers, may also be value of in early identification of IRA {Infarct Related Artery}, total CK activity, CK-MB isoenzymes appear to be the most promising biochemical markers.

In addition, the thresholds suggested for the diagnosis of reperfusion were generally derived from “time-to-peak” values. This rules out early diagnosis because peak CK plasma values are reached, on averages 9 -+ 6 hours after thrombolysis.

Determination of plasma total and MB CK concentration provides accuracy superior to any other currently available method for the diagnosis of acute MI.

 In addition to providing precise diagnosis of acute MI, quantitative MB CK assays can also be used to obtain an accurate estimate of infarct size. In recent years, accuracy in the diagnosis of acute MI has assumed even greater importance, since the choice and timing of a variety of diagnostic and therapeutic options following coronary care unit admission hinge on whether infarction has occurred. Furthermore, the advent of thrombolytic therapy of acute MI has emphasized the need for more sensitive biochemical markers of necrosis in the first hours. The eventual realization that the reestablishment of blood flow was the dominant mechanism for the diminution of infarct size led to a therapeutic approach dominated by thrombolysis and more literally by the use of interventions to open vessels and maintain them open.

The key observation is that benefit by the use of a drug could be demonstrated if the drug was given prior to the period of ischemia. 

Nevertheless, the greatest benefit in the management of patients with myocardial infarction ha unquestionably been the reestablishment of blood flow as early as possible after occlusion

The aim of this study is to determine the reperfusion of injury exacerbated by thrombolytic drugs in Myocardial Infarction through the process of elevation of cardiac enzymes which peaks and comes to normal levels within 24 hours, preventing prolonged injury and ischemia of myocardial tissue.

However, the aim was to evaluate prospectively biochemical markers for the diagnosis of coronary patency early after IV thrombolysis for Acute Myocardial Infarction.


“The effect of thrombolytric drugs on cardiac enzymes, Creatine Phospho kinase and Creatine Kinase -MB, in myocardial Infarction”.


  • To evaluate the effect of thrombolytic drugs on cardiac enzymes.
  • To compare the effect of thrombolytic drugs and non thrombolytic drugs on cardiac enzymes
  • To determine the importance of thrombolytics for a patient with myocardial infarction
  • To suggest teaching guidelines to public regarding early seeking of medical help at the onset of chest pain.


Effect: Result or produce a result

Thrombolytic drugs: medications used to dissolve blood clots

CPK: A cardiac isoenzyme which releases into the blood in high levels when an injury occurs to the heart. It is also known as Creatine Kinase or Creatine Phophokinase.

CK-MB: It is also a cardiac isoenzyme releases into the blood from the heart muscle during an injury of the heart

Myocardial infarction: Necrosis of a region of the myocardium caused by an interruption in the supply of blood to the heart, usually as a result of occlusion of a coronary artery.


"Thrombolytic agents has effect on fall in peak levels on cardiac enzymes, CK and CK-MB"


Coronary care unit: The data of this research is applicable in the settings of coronary care unit.

Age: Clients are selected only between 35 to 65 yrs of age.

Myocardial infarction: This is also applicable to the clients who were admitted in the hospital within 6 hours of the onset of the chest pain with myocardial infarction who received Inj. Metalyse.

Acute coronary syndrome: The clients who are admitted after 6 hours of the onset of the chest pain with acute coronary syndrome are included in the control group.


This study was done by an experimental method of research design in the settings of Coronary Care Unit in Dubai Hospital, U.A.E. A consecutive series of patients receiving IV Metalyse [ Tenecteplase ]  for MI from May 2006 to November 2006 were included in this study.


This study uses the  comparative design.


This study was conducted in patients irrespective of age, sex and nationality, who were admitted in Coronary Care Unit through Emergency Department in Dubai Hospital, U.A.E.


This study included 60 clients, men and women, irrespective of nationalities, between 35 years to 65 years of age.  Among 60 clients 30 were taken as experimental group and another 30 considered as control group.


The samples are selected as convenient sample, into two groups, the experimental and control groups. The clients who received thrombolytic agents within 6 hours of the onset of the chest pain are selected as an experimental group, and the clients who were presented late after 6 hours of the onset of the chest pain and not received thrombolytics, are selected as control group. All patients treated had the diagnosis of myocardial infarction confirmed by subsequent elevation of both Creatine Kinase [CK] and CK-MB isoenzymes levels. IV Metalyse is administered at a dose of 6000 units to 9000 units according to the weight of the patients. Patients with acute MI who were admitted to CCU more than 6 hours of onset of pain were also included.


Data for the study is collected by an instrument, which consists of 22 items including sample number, age, and sex. Religion, nationality, occupation, food habits, life style onset of chest pain, date and time of admission, signs and symptoms, vital signs, type of MI, protocol of thrombolytic therapy, levels of cardiac enzymes, post thrombolytic treatment, drugs received and date of discharge.

Study reveals that, majority of the clients who had MI was from the Indian subcontinents, constituting 63.3 % and the minority constituting just 1.6 %, from Great Briton and Turkey. 3.3 % of the clients were Egyptians and Syrians. Bangladeshis comprised, 6.6 % and Pakistanis were about 21.6 %. Only 9.9 % of the clients who had MI were Dubai Nationals. Among them 46.6% of the clients were aged between 46 – 55 years and 41.6 % of the clients were between 36 – 45 years and the remaining 11.6 % of the clients are between 56 – 65 years of age.

36.2 % of the clients had acute coronary syndrome and were not given thrombolytics. Remaining of the clients was with true MI and most of them were thrombolysed. However, all clients have undergone coronary angioplasty. Out of these clients only one client had normal coronary vessels, two were with mild coronary stenosis for conservative medical treatment and 4 clients with major triple vessel block were posted for CABG. Rest of the clients was treated with Percutaneous Coronary Angioplasty to LAD [50%], RCA [21.6%] and Circumflex [13.5%].

It is also evident from the study that most of the Indians are affected with MI and the major contributing factors are smoking, stress and lack of knowledge about the disease condition.

Based on Chi-Square deviation the association between normalization of cardiac enzymes levels in the study groups are as follows-

In Experimental group, 30 clients have received Inj. Metalyse . among them except 4 clients, remaining 26 clients reports seen that cardiac enzymes are normalized within 24 hours after the admission and administration of thrombolytic agent.

In control group, 30 clients blood reports for normalization of cardiac enzymes were anlysed, where we found 27 clients reports shown the higher levels of cardiac enzymes after 24 hours of the admission.

  1. Critical Value 14.56,    P value < 0.05 and Null hypothesis rejected

Inj. Metalyse has a good effect on the cardiac muscle provided with Critical Value- 14.56, Probability Value- < 0.05, as evidenced by fall in peak levels of cardiac enzymes CK and CK-MB within 24 hours after received thrombolytic agent.


Tenecteplase [ Metalyse] is a recombinant fibrin-specific plasminogen activator. It binds to the fibrin component of the thrombus and selectively converts thrombus-bound plasminogen to plasmin, which degrades the fibrin matrix of the thrombus. Tenecteplase is cleared from the circulation by binding to specific receptors in the liver followed by catabolism to small peptides.

After single intravenous bolus injection of tenecteplase in patients with acute myocardial infarction, tenecteplase antigen exhibits biphasic elimination from plasma. There is no dose dependence of tenecteplase clearance in the therapeutic dose range.

The initial dominant half-life is 24+_5.5 [mean=/-SD] min. the terminal half-life is 129+_87 minutes, and plasma clearance is 119+_49 ml/min

The main finding of this study is the early peaking of the total CPK level and CK-MB

isoenzymes have identified with successful reperfusion after Metalyse therapy. The peak CPK levels reached in 12 hours and CK-MB levels were shifted in 6 hours. The study reveals that the cardiac enzymes levels peaked and normalized within 24 hours time in the experimental group who received Thrombolytic agents within 6 hours of the onset of the chest pain. Where as it took 3- 5 days for the enzyme levels to peak for clients in the control group, who did not receive thrombolytic agents due to late arrival to the hospital, resulting in more damage to the myocardium.

Thus, it is evident that the extent of injury to the myocardium as well as the oxygen demand is less in the experimental group of the clients. 

Finally, it may be used as a surrogate end point for angiographic demonstration of

patency in future clinical studies of reperfusion therapy. Diagnostic performance improved when the analysis was restricted to patients treated >6 hours after the onset of symptoms.


Clinical studies of fibrinolytic therapy in myocardial infarction show, that early thrombolytic treatment starting within 6 hours of the onset of the chest pain, significantly decreases the risk of further damage of the myocardium and oxygen demand, by the process of fall in peak levels of cardiac enzyme levels within 24 hours.

Inj. Metalyse has early peaking of cardiac enzymes in experimental group reflect the Infarction Related Artery opened, the clot has dissolved by Inj. Metalyse which means we have good thrombolytic effect, that is why we have early peaking levels.

Early identification of patients with persistent occlusion after thrombolyis during

Acute Myocardial Infarction also is important because it can pave the way for rescue interventions such as rescue Percutaneous Transluminal Coronary Angioplasty or repeated thrombolysis.



Determine intensity of client’s angina

Observe for signs and symptoms

Place patient in a comfortable position

Administer oxygen if required

Obtain vital signs every 15 minutes for 2 hours, every half an hour for one hour and

every hour for two hours then as required

Obtain a 12 lead ECG

Monitor for relief of pain

Monitor patient’s response to drug therapy

Institute continuous cardiac monitoring and observe for- reperfusion, arrhythmias, rhythm changes, bradycardia and tachycardia

Interpret rhythm strips

Watch for complaints of headache with use of nitrates

Watch for recurrences of pain. Reinforce the importance of notifying nursing staff whenever pain is experienced.

Administer medications to relieve patient’s anxiety as directed such as sedatives and  tranquilizers

Provide complete bed rest for 24 hours

Determine level of activity that precipitated anginal pain occurs.

Identify specific activities patient may engage in that are below the level at which anginal pain occurs

Prepare for the diagnostic and treatment procedures such as coronary angiogram and PTCA [ Percutaneous Transluminal Coronary Angioplasty]


Counsel on risk factors and life style changes such as-

Methods of stress reduction such as biofeedback and relaxation techniques

Low fat and low cholesterol diet

Avoid excessive caffeine intake

Do not use diet pills, nasal decongestants

Follow up visits to control diabetes and hypertension

Educate patient and family members regarding-

Prevention of recurrence of pain

Regular use of medications

Hazards of smoking

Prevention of other contributing factors

Regular follow up

Importance of dietary modifications

Avoiding activities which cause anginal pain such as sudden exertion, walking against the wind, extremes of temperature, emotionally stressful situations, refraining from engaging in physical activity for 2 hours after meals, reduce weight etc.

Appropriate use of medications

Side effects of medications


Lead interdisciplinary intervention programs

Education of nursing students and staff

Provide in-service nursing education

Maintenance of records and reports

Maintenance of statistics

Making of policies and procedures

Supervision and evaluation of staff performance

Recommendations for further study

A majority of post MI patients actually not participating in formal cardiac rehabilitation programs due to either lack of structured programs, physician

referrals, low patient motivation, non compliance and financial constraints.

Cardiac rehabilitation provides a venue for continued education, reinforcement

of life style modification and adherence to comprehensive prescriptions of

therapies for recovery for MI, which includes exercise training.

Participation in cardiac rehabilitation programs, post MI with a decrease in

subsequent cardiac morbidity and mortality.

Adequate education in the hospitals and work places on causative and contributing factors, preventive measures of heart attacks and re heart attacks, is necessary.

All forms of reperfusion, depending on local facilities, need to be available to patients. Protocols must be written and agreed for the strategy of reperfusion to be applied within a network. Early diagnosis of ST Elevation Myocardial Infarction is essential and is best achieved by rapid ECG recording and interpretation at first medical contact, wherever this contact takes place. 

Can Heart Attacks Be Predicted To Save Lives?

About one of every five deaths in the United States are attributed to heart diseases. However, scientists may now well be on their way to make heart attack prediction possible so that many lives can be saved.

Heart disease is term used for a range of different diseases affecting the heart. They are often treated by surgery and cardiovascular drugs.

Even though from 1995 to 2005 the death rate from heart disease declined 34 percent, there still is a lot of potential for it to decrease further with the aid of technology. A device is being tested to monitor the heart and raise a red flag in time so that early help can be sought.

The Life Saving Technology

Called the AngelMed Guardian system, the device is about the size of a standard pacemaker is meant to be installed inside the skin close to the collarbone with a wire placed in the right chamber of the heart.

It comprises an external telemetry device and and a programmer meant to help the medics assess the heart signals. The job of the device will be to monitor a person’s heart’s activity for signs that may indicate an impending heart attack.

As soon as the implanted diagnostic equipment finds that something’s gone amiss inside the heart, making use of Bluetooth technology and pagers, it will sound an alert to others so that quick medical attention can be provided to the patient. Also, the more disturbing or acute the symptoms of an upcoming heart attack, stronger the alert this device transmits.

According to experts, the maximum damage to the heart occurs during the first two hours after a coronary gets blocked during a heart attack. And most of the time patients take about three hours to recognize an oncoming heart attack, so help often reaches late to the sufferers. However, the unique ability of this device is that it can recognize the warning signs and sound an alert hours before the attack actually occurs thus helping doctors save lives.

Still undergoing Phase II clinical trials, if all goes well then it may actually be able to predict heart attacks and save lives.

Coronary Artery Disease – Causes, Symptoms and Treatments

CAD (Coronary Artery Disease) refers to the contracting of the heart arteries because of atherosclerosis. The heart muscle doesn’t get sufficient oxygen when the heart arteries are contracted. If your heart is starving out of oxygen, then the pain in the chest arises which is called as angina. If your artery is totally blocked then the result would be heart attack. In medical terms, the heart attack is referred as myocardial infarction (MI). Coronary Artery Disease is considered to be the most usual type of the heart disease and the heart attack has been considered to be leading killer for both men as well as women.

Many of such deaths could be prevented by taking in control few risk factors which might lead to CAD. Few of such risk factors which need to be controlled are high blood pressure, diabetes and high blood cholesterol. There’re other risk factors that are required to be controlled related to our lifestyle, like quit smoking, maintain a perfect weight as well as start including physical activities or exercise in your daily routine.

Even though today there are numerous treatment coming up for heart disease, but the main way of preventing death and illness from Coronary Artery Disease is by controlling the risk factors.

Coronary Artery Disease causes are:

Mostly the heart faces lower oxygen supply because of atherosclerosis and this is even termed as hardening of the arteries. At the time of such condition, plaques which are actually fatty deposits get formed in the blood vessels’ linings. These plaques (at the time of formation) make your arteries narrow and because of this only few amount of blood vessel is able to reach the heart, therefore the supply of oxygen also gets lessen. Atherosclerosis arise frequently because of more amount of bad cholesterol as well as triglycerides that circulate in your bloodstream.

Coronary Artery Disease Symptoms –

Few of the individuals with Coronary Artery Disease may contain no symptoms unless this disease has become serious enough and might cause pains in their chest, or say angina pectoris.

Angina being stable is frequently considered as the very 1st symptom from which a person can find out that he or she is suffering from CAD. Discomfort or chest pain may occur due to the activity and might disappear when they take proper rest. If the angina is unstable then it could be difficult to predict the disease and could rise when one is relaxing. This indicates the fast progression of Coronary Artery Disease and there are superior chances of heart attack as well as one must meet the physician immediately.

Coronary Artery Disease Treatments –

A doctor could suggest any of the following treatments –

– Cholesterol lowering medications could decline the bad cholesterol level which is present in ones blood by increasing the good cholesterol level.

– Antiplatelet medication doesn’t allow the clots to form.

– Blood pressure declining agents could decline the heart attack risk dramatically when one has superior blood pressure.

If you believe to have that disease please consult a doctor.

To Your Health!