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 !!!!!!!!!!!!!!!!!!!!!!!!

what is it ????

Refers to diabetes mellitus or, less often, to diabetes insipidus. Diabetes mellitus and diabetes insipidus share the name “diabetes” because they are both conditions characterized by excessive urination (polyuria).

The word “diabetes” is borrowed from the Greek word meaning “a siphon.” The 2nd-century A.D. Greek physician, Aretus the Cappadocian, named the condition “diabetes.” He explained that patients with it had polyuria and “passed water like a siphon.”

When “diabetes” is used alone, it refers to diabetes mellitus. The two main types of diabetes mellitus — insulin-requiring type 1 diabetes and adult-onset type 2 diabetes — are distinct and different diseases in themselves.

What are the Types ???

1.  Type I

2. Type II

3. Gestational Diabetes Mellitus

4. Others

Type I ????

It is also called Insulin Dependent Diabetes (IDDM) or Juvenile Diabetes.

Although, it may occur at any age, but it usually develops in childhood or adolescence, before the age of 25. Equal incidences are seen in both sexes. But there are increased incidences in white population. This type of diabetes accounts for 10-15% of all cases of Diabetes mellitus. This type of Diabetes is acute in onset and progresses rapidly.

Type 1 Diabetes is caused by complete deficiency of Insulin resulting from Beta cell destruction. It can be explained on the basis of three basic factors:

(i) Genetic susceptibility:

(ii) Auto Immunity:

(iii) Environmental Factors:

It may be:

• Viral infections such as –congenital Rubella, Mumps, Measles and coxsackie B virus may lead to the onset of Type 1 Diabetes.
• Exposure to cow’s milk rather then material milk in infancy may lead to development of type 1 DM. It is because the albumin from cow’s milk may react with islet cells of pancreas, leading to their destruction.
• Geography also plays an important role, as the incidences of Type 1 DM are mainly high in Finland and Sardinia

Type II??

This type of Diabetes is also known as Adult onset Diabetes. Non-insulin dependent Diabetes Mellitus (NIDDM), Maturity onset diabetes.

It is more common and constituents 80-90% of all cases of diabetes. It usually occurs in adults over 40 years of age. But now a day few cases are observed in teen years also. Many people with Type 2 diabetes do not known they have it, although it is a serious condition. Generally, when the diagnosis is made, patient is asymptomatic. Routine urine or blood test shows the presence of high glucose levels in the blood or urine. The onset of symptoms in type 2 are slow and does not progresses rapidly.

The main cause of Type 2 Diabetes mellitus is insufficient Insulin secretion by Beta Cells due to their destruction. Due to lack of insulin, there is raised blood sugar level and finally diabetes” type 2 diabetes mellitus also occur due to development of Insulin Resistance where the cells of the body mainly fat and muscle cells does not accept the insulin. The liver of such patients also produces glucose through a process called gluconeogenesis, which further worsens the controlling of glucose level.

Type 2 diabetes is more prevalent because of faulty eating habit, increasing obesity end failure to exercise. There is a direct relationship between the degree of obesity and the risk of developing type 2 diabetes. The chance to become 2 diabetes doubles for every 20% increase form normal body weight. Heredity and Genetic factors play a major role in development of Type-2 Diabetes.

In Europe and North America about 80% of all diabetes have Type-2 Diabetes have Type 2 Diabetes mellitus.

Gestational Diabetes Mellitus (GBM)

Gestational diabetes mellitus (GDM) is defined as any degree of glucose intolerance, with the onset of pregnancy. Women who develop Type –1 diabetes mellitus during pregnancy and women with undiagnosed a symptomatic type –2 diabetes mellitus that is discovered Gestational Diabetes Mellitus. Women with diabetes mellitus before pregnancy are said to have “Pregestational Diabetes”. Many women who have developed gestational diabetes may have controlled glucose level during the first half of the pregnancy and develop insulin

deficiency during the latter half of the pregnancy, leading to hyper-glycaemia.

Gestational Diabetes Mellitus is a complication in approximately 4% of all pregnancies in the United States. Mother with Gestational diabetes mellitus have increased rate of caesarian delivery and chronic hypertension “High blood Glucose levels in early pregnancy may deprive the embryo of oxygen and lead to Birth Defects, especially of the heart and spinal cord. Maintaining blood glucose control continues to be important throughout the pregnancy, but it is particularly important during the first eight weeks, when an embryo’s organs are farming.

To diagnose GDM, a 50 gm glucose-screening test should be performed at 24-28 weeks of gestation known as Glucose Tolerance Test (GTT). By them, the placenta begins to make the hormones that lead to insulin resistance. The screening test measures the blood sugar response to glucose consumed in a drink. Untreated gestational diabetes can lead to problems for both the mother and the child. It can lead to Fat baby syndrome or Microsomatia, in which the baby’s body produces extra fat.

Others ???

Diabetes mellitus of various known reasons is included in this type. It includes:

It is also seen during natal and early childhood.

Treatment ???

Controlling your blood sugar is essential to feeling healthy and avoiding long-term complications of diabetes. Some people are able to control their blood sugar with diet and exercise alone. Others may need to use insulin or other medications in addition to lifestyle changes. In either case, monitoring your blood sugar is a key part of your treatment program.

A healthy diet and exercise should be placed as a priority for diabetes treatment.  Second, you might also try some of the diabetes treatment using alternative medicine.  Third, follow your doctor’s prescriptions.  And last, pancreas or islet cell transplantation may be an option for people whose kidneys are failing or who aren’t responding to other treatments.

1. Monitoring Blood Sugar

a. Food

b. Exercise and Physical activity

c. Medications

d. Illness

e. Alcohol

f. Hormonal Imbalance

2.  Healthy Diet

3.  Healthy Weight

4. Medications

a. Sulphonylurea Drugs

b. Meglitinide

c. Biguanides

d. Apha Glycosidase inhibitors

e. Thiozolidinediones

5. Pancreas transplant

Other Treatment Available !!!

1. Accupunture

2. Biofeedback

3. Chromium

4. Magnesium

5. Vanadium

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.

What is it ???

Impotence is a medical condition that affects a male’s ability to get or sustain an erection. It is often called erectile dysfunction, as it usually only affects erectile ability, which distinguishes it from other male sexual problems of both physical and psychological natures. Causes of impotence are typically physical, but in some cases it may also be caused or aggravated by psychological issues.

CAUSES???

Impotence is a medical condition that affects a male’s ability to get or sustain an erection. It is often called erectile dysfunction, as it usually only affects erectile ability, which distinguishes it from other male sexual problems of both physical and psychological natures. Causes of impotence are typically physical, but in some cases it may also be caused or aggravated by psychological issues. Medical treatment for this problem is now widely available, and widely used.

Psychological  causes???

- Stress and anxiety
- Fear of failure
- Problems with your relationship

Some people may wonder why they need to take medicines for a condition that doesn’t have symptoms and doesn’t appear to affect their quality of life. Your doctor is aware of this and will try to avoid treatments that make you feel bad or interfere with your lifestyle. Although taking medication may seem like a chore, it is being prescribed to prevent serious illness or even death. Always take medicines according to instructions, and do not stop taking them abruptly as this can cause problems. If you have any questions about your medicine, always ask your doctor.

Impotence can nearly always be treated – 95 percent of men find a suitable treatment. The simplest are talking therapies, such as cognitive behavioural therapy, and medicines.If the cause is mainly because you are anxious or are having relationship difficulties, then talking to a counsellor or psychosexual therapist will probably be most helpful for you.

Risk factors ??

1. Chronic health conditions

People suffering from chronic diseases have a high risk of erectile dysfunction. Chronic diseases such as:
a) Heart diseases are caused by cholesterol building up in the arteries and blood vessel resulting in inadequate blood flow into the penis.
b) Diabetes with unhealthy diet causes high levels of glucose build-up in the bloodstream resulting in narrowed arteries and blood vessels that prevent adequate blood from entering the penis.
c) Prostate enlargement and chronic prostate: Inflammation of the prostate also reduces the blood flow entering the penis resulting in erectile dysfunction.
Other chronic diseases affecting organs like the lung, liver, and kidney also can lead to erectile dysfunction because of inflammation, inadequate blood flow or hormonal imbalance.

2. Aging

Aging results in more testosterone to be converted to dihydro-testosterone causing erections to take longer to develop and to need more direct touch to the penis.

3. Nerve damage

It is obvious that any damage to the nerve that directly controls erections can cause temporarily erectile dysfunction.

4. Medication

The side effects of some medications used to treat high blood pressure, depression, and prostate enlarged may interfere with nerve impulses and reducing the blood flow to the penis.

5. Prolong cycling

Prolong cycling over an extended period and pressure from a bicycle seat compresses nerves and blood flow to the penis, leading to temporary erectile dysfunction.

6. Psychological conditions

Other psychological conditions such as depression, anxiety and stress also contributes to some cases of erectile dysfunction.

7. Substance abuse

Substance abuse such as smoking, alcohol, marijuana or other drugs often causes erectile dysfunction.
There are many other risk factors such as obesity, diabetes, high levels of cholesterol and triglycerides that can cause erectile dysfunction.

Treatment ???

1)Sexual counselling

2)Oral Medication :

The introduction of Viagra by Pfizer in March, 1998,, marked the beginning of a revolution in the oral medical management of erectile dysfunction (ED, E.D., impotence). The launch of Viagra was soon followed by that of Levitra and Cialis. Other (even better) drugs are in the pipeline.Effective oral medication has re-written the management of ED and is effective in nearly 70 – 75 % of cases. Several internet resources are available for more detailed information about these drugs and these will not be discussed in detail here.

3)Hormone Replacement therapy:

Testosterone is the major male hormone that gives men their sexual characteristics (deep voice, beard, chest hair). As men age, their level of testosterone decreases (andropause) and this may have an adverse effect on sexual performance. In proven cases of andropause, testosterone preparations may enhance potency and improve sex drive. However, this therapy must be only offered under expert medical supervision because many side effects can occur.

4)External Vaccum Devices

vacuum device, and one or more tension rings. This therapy is purported to be effective for over 90% of the men who use it. In fact, most can technically master its use in one day, and can use it to maintain erections for up to 30 minutes, even after ejaculation and/or orgasm.

Prevention  of Impotence????

There is no specific treatment to prevent impotence. Perhaps the most important measure is to maintain general good health and avoid atherosclerosis by exercising regularly, controlling weight, controlling hypertension and high cholesterol levels, and avoiding smoking. Avoiding excessive alcohol intake may also help.