Top Hair Care Tips

Hair is more than just about preserving our body heat. It’s one of the first features other people notice about us so we use it pretty much as a canvas with which to stamp our own personal style, hide certain facial flaws or highlight our best assets. Because of the importance of hair as a sexual attraction tool, we are willing to splurge on a plethora of styling and hair dying products that eventually damage hair cuticles, making a once shiny, lustrous, healthy hair into a dry, frizzy mass of split ends.

Dermatologist Zoe D Draelos reveals some facts you may not know about hair and ways to keep it up in tip-top shape :Hair in our 20sHair is at the healthiest when we’re in our 20s but then this is also the age during which many women fall victims to fad diets. Nourished hair needs protein, vitamins and minerals and if it doesn’t get enough nutrients, hair will lose sheen and lustre and will look dull and brittle. Also since meat is a great source of protein, Draelos advises vegetarians to supplement meat with dairy products like cheese, yoghurt and milk. Hair in our 30sPregnancy is a common event for women in their 30s and during the pregnancy state, hair is in excellent condition but hair starts to fall off six months after birth. While hair will eventually grow back for most women, women who have a female-pattern hair loss may not be as lucky. Hair in our 40sSo begins the disguising of grey hairs. Draelos says that dying our hair is damaging but if you have to dye your hair, use a colour within three shades of your natural hair colour, especially if the desired colour is lighter. Getting our hair dyed more than 3 shades lighter usually needs the assistance of peroxide which everyone knows is a murderer of healthy hair. Also at this time, women enter the periomenopause stage during which estrogen levels decrease, resulting in thinning of hair (decrease in hair diameter). Hair doesn’t grow as quickly, if at all. Hair in our 50sAs hair continues to thin, Draelos suggests women should decrease the amount of time they leave in styling products like hairspray and hair dyes and to use protein-conditioners that can strengthen hair by up to 10%. Draelos’ biggest tip is to do as little as possible to your hair. Using too many styling products and subjecting your hair to various treatments can do much more damage than sticking to the basic routine of shampooing and conditioning. Other tips from haircare websites : From http://www.salonweb.com/pro/shampoo.htm–* check the ingredients of your shampoo and opt for an ingredient called sodium laurel sulfate which is gentle on your hair and won’t leave it dry. * to prevent or help damaged hair : - use thermal protector when using heating products- do not blow dry hair completely but leave some moisture in- blow dry on a cool setting- use low or no ammonia hair colour- comb through wet hair & never use a brush- eat protein-rich foods like chicken, fish and nutsFrom http://www.free-beauty-tips.glam.com/–* treating dandruff : - try a vinegar wash (mix 2 teaspoons of vinegar with 6 teaspoons of water. Apply to scalp and keep it in by wrapping a towel around your head before going to bed. In the morning, apply the mixture again then rinse. No need to worry about any smell as the smell of vinegar will evaporate quickly.

Health and Beauty

At what age would you take your daughter to a beauty spa?
November 29th 2007 01:26
In the US, girls as young as 6 can waltz into a beauty salon, ask for a facial, manicure and hair extensions without the beauty therapist batting an eyelid or quickly shepherding them out of the salon to look for their parents. Because the thing is, it’s actually the mothers ushering their daughters into these pampering sessions, which some of us didn’t get until we were adults, under the guise of quality time.

http://www.healthandbeauty.net.au/

COPD(Chronic obstructive pulmonary disease)

For COPD occuring in horses, see recurrent airway obstruction.
Chronic obstructive pulmonary diseaseClassification & external resources
Chronic obstructive pulmonary disease (COPD), also known as chronic obstructive airway disease (COAD), is a group of diseases characterized by the pathological limitation of airflow in the airway that is not fully reversible. COPD is the umbrella term for chronic bronchitis, emphysema and a range of other lung disorders. It is most often due to tobacco smoking,[1] but can be due to other airborne irritants such as coal dust, asbestos or solvents, as well as congenital conditions such as alpha-1-antitrypsin deficiency.

From Wikipedia, the free encyclopedia
(Redirected from COPD)

1. Signs and symptoms

Signs and symptoms
The main symptoms of COPD include dyspnea (shortness of breath) lasting for months or perhaps years, possibly accompanied by wheezing, and a persistent cough with sputum production.[2] It is possible the sputum may contain blood and become thicker (hemoptysis), usually due to damage of the blood vessels of the airways. Severe COPD could lead to cyanosis (bluish decolorization usually in the lips and fingers) caused by a lack of oxygen in the blood. In extreme cases it could lead to cor pulmonale due to the extra work required by the heart to get blood to flow through the lungs.[3]
COPD is particularly characterised by the spirometric measurement of a ratio of forced expiratory volume over 1 second (FEV1) to forced vital capacity (FVC) being < title="FEV1" href="http://en.wikipedia.org/wiki/FEV1">FEV1 < title="" href="http://en.wikipedia.org/wiki/COPD#_note-2">[4] as measured by a plethysmograph. Other signs include a rapid breathing rate (tachypnea) and a wheezing sound heard through a stethoscope. Pulmonary emphysema is NOT the same as subcutaneous emphysema, which is a collection of air under the skin that may be detected by the crepitus sounds produced on palpation.[5]

2. Causes

aigarette smoking
A primary risk factor of COPD is chronic tobacco smoking. In the United States, around 80 to 90% of cases of COPD are due to smoking.[6] Not all smokers will develop COPD, but continuous smokers have at least a 25% risk.[7]

Occupational pollutants
Some occupational pollutants, such as cadmium and silica, have shown to be a contributing risk factor for COPD. The people at highest risk for these pollutants include coal workers.

Air pollution
Urban air pollution may be a contributing factor for COPD as it is thought to impair the development of the lung function. In developing countries indoor air pollution, usually due to biomass fuel, has been linked to COPD, especially in women.[1]

Genetics

Very rarely, there may be a deficiency in an enzyme known as alpha 1-antitrypsin which causes a form of COPD.[8]

Other risk factors
Increasing age, male gender, allergy, repeated airway infection and general impaired lung function are also related to the development of COPD.

8 Prognosis

The NIH IPAH registry from the 1980's showed an untreated median survival of 2-3 years from time of diagnosis, with the cause of death usually being right ventricular failure (cor pulmonale). Although this figure is widely quoted, it is probably irrelevant today. Outcomes have changed dramatically over the last two decades. This may be because of newer drug therapy, better overall care, and earlier diagnosis (lead time bias). A recent outcome study of those patients who had started treatment with bosentan (Tracleer®) showed that 89% patients were alive at 2 years.[13] With multiple agents now available, combination therapy is increasingly used. Impact of these agents on survival is not known, since many of them have been developed only recently. It would not be unreasonable to expect median survival to extend past 10 years in the near future.[14]

7.Treatment

Treatment is determined by whether the PH is arterial, venous, hypoxic, thromboembolic, or miscellaneous. Since pulmonary venous hypertension is synonymous with congestive heart failure, the treatment is to optimize left ventricular function by the use of diuretics, beta blockers, ACE inhibitors, etc., or to repair/replace the mitral valve or aortic valve.
In PAH, lifestyle changes, digoxin, diuretics, oral anticoagulants, and oxygen therapy are considered conventional therapy, but have never been proven to be beneficial in a randomized, prospective manner.
High dose calcium channel blockers are useful in only 5% of IPAH patients who are vasoreactive by Swan-Ganz catheter. Unfortunately, calcium channel blockers have been largely misused, being prescribed to many patients with non-vasoreactive PAH, leading to excess morbidity and mortality. The criteria for vasoreactivity have changed. Only those patients whose mean pulmonary artery pressure falls by more than 10 mm Hg to less than 40 mm Hg with an unchanged or increased cardiac output when challenged with adenosine, epoprostenol, or nitric oxide are considered vasoreactive. Of these, only half of the patients are responsive to calcium channel blockers in the long term.

[edit] Vasoactive substances
Many pathways are involved in the abnormal proliferation and contraction of the smooth muscle cells of the pulmonary arteries in patients with pulmonary arterial hypertension. Three of these pathways are important since they have been targeted with drugs — endothelin receptor antagonists, phosphodiesterase type 5 inhibitors, and prostacyclin derivatives.

[edit] Prostaglandins
Prostacyclin (prostaglandin I2) is commonly considered the most effective treatment for PAH. Epoprostenol (synthetic prostacyclin, marketed as Flolan®) is given via continuous infusion that requires a semi-permanent central venous catheter. This delivery system can cause sepsis and thrombosis. Flolan® is unstable, and therefore has to be kept on ice during administration. Since it has a half-life of 3 to 5 minutes, the infusion has to be continuous (24/7), and interruption can be fatal. Other prostanoids have therefore been developed. Treprostinil (Remodulin®) can be given intravenously or subcutaneously, but the subcutaneous form can be very painful. An increased risk of sepsis with intravenous Remodulin® has been reported by the CDC. Iloprost (Ilomedin®) is also used in Europe intravenously and has a longer half life. Iloprost (marketed as Ventavis®) is the only inhaled form of prostacyclin approved for use in the US and Europe. This form of administration has the advantage of selective deposition in the lungs with less systemic side effects. Oral and inhaled forms of Remodulin® are under development. Beraprost is an oral prostanoid available in Japan and South Korea.

[edit] Endothelin receptor antagonists
The dual (ETA and ETB) endothelin receptor antagonist bosentan (marketed as Tracleer®) was approved in 2001. Sitaxsentan, a selective endothelin receptor antagonist that blocks only the action of ETA, has been approved for use in Canada, Australia, and the European Union, to be marketed under the name Thelin®.[10] Sitaxsentan has not been approved for marketing by the US FDA. A new trial to address the FDA's concerns will begin in 2008. A similar drug, ambrisentan is marketed as Letairis® in U.S. by Gilead Sciences.[11] In addition, another dual/nonselective endothelin antagonist, Actelion-1, from the makers of Tracleer®, will enter clinical trials in 2008.

[edit] Phosphodiesterase type 5 inhibitors
Sildenafil, a selective inhibitor of cGMP specific phosphodiesterase type 5 (PDE5), was approved for the treatment of PAH in 2005. It is marketed for PAH as Revatio®. Tadalafil (currently marketed as Cialis® for erectile dysfunction) is currently finishing its Phase III clinical trials and results should be reported very soon.

[edit] Other agents
Vasoactive intestinal peptide by inhalation should enter clinical trials for PAH in 2008. PRX-08066 is a serotonin antagonist currently being developed for hypoxic pulmonary hypertension. A recent study showed benefit as measured by echocardiography. A study using cardiac catheterization with a Swan-Ganz catheter is underway.

[edit] Surgical
Atrial septostomy is a surgical procedure that creates a communication between the right and left atria. It relieves pressure on the right side of the heart, but at the cost of lower oxygen levels in blood (hypoxia). It is best performed in experienced centers. Lung transplantation cures pulmonary arterial hypertension, but leaves the patient with the complications of transplantation, and a post-surgical median survival of just over five years.[12]
Pulmonary thromboendarterectomy (PTE) is a surgical procedure that is used for chronic thromboembolic pulmonary hypertension. It is the surgical removal of an organized thrombus (clot) along with the lining of the pulmonary artery; it is a very difficult, major procedure that is currently performed in a few select centers. Case series show remarkable success in most patients.
Treatment for hypoxic and miscellaneous varieties of pulmonary hypertension have not been established. However, studies of several agents are currently enrolling patients. Many physicians will treat these diseases with the same medications as for PAH, until better options become available. Such treatment is called off-label use.

6.Epidemiology

IPAH is a rare disease with an incidence of about 2-3 per million per year and a prevalence of about 15 per million. Women are almost three times as likely to present with IPAH than men.
Other forms of PAH are far more common. In scleroderma the incidence has been estimated to be 6 to 60% of all patients, in rheumatoid arthritis up to 21%, in systemic lupus erythematosus 4 to 14%, in portal hypertension between 2 to 5%, in HIV about 0.5%, and in sickle cell disease ranging from 20 to 40%.
Diet pills such as Fen-Phen produced an annual incidence of 25-50 per million per year.
Pulmonary venous hypertension is exceedingly common, since it occurs in most patients symptomatic with congestive heart failure.
Up to 4% of people who suffer a pulmonary embolism go on to develop chronic thromboembolic disease including pulmonary hypertension.
Only about 1.1% of patients with COPD develop pulmonary hypertension with no other disease to explain the high pressure. Sleep apnea is usually associated with only very mild pulmonary hypertension, typically below the level of detection. On the other hand Pickwickian syndrome or obesity-hypoventilation syndrome is very commonly associated with right heart failure due to pulmonary hypertension.

5.Classification

Current classification
In 2003, the 3rd World Symposium on Pulmonary Arterial Hypertension was convened in Venice to modify the classification based on the new understanding of disease mechanisms. The revised system developed by this group provides the current framework for understanding pulmonary hypertension.
The system includes several improvements over the former 1998 Evian Classification system. Risk factor descriptions were updated, and the classification of congenital systemic-to pulmonary shunts was revised. A new classification of genetic factors in PH was recommended, but not implemented because available data were judged to be inadequate.
The Venice 2003 Revised Classification system can be summarized as follows:[9]
WHO Group I - Pulmonary arterial hypertension (PAH)
WHO Group II - Pulmonary hypertension associated with left heart disease
WHO Group III - Pulmonary hypertension associated with lung diseases and/or hypoxemia
WHO Group IV - Pulmonary hypertension due to chronic thrombotic and/or embolic disease
WHO Group V - Miscellaneous

[edit] Previous terminology
The terms primary and secondary pulmonary hypertension (PPH and SPH) were formerly used to classify the disease. This led to the assumption that only the primary disease should be treated, and the secondary variety should be ignored in favor of treating only the underlying illness. In fact all forms of pulmonary arterial hypertension are treatable. Unfortunately, this classification system still persists in the minds of many physicians, and probably leads to many patients with being denied treatment. This approach to pulmonary arterial hypertension may also contribute to underdiagnosis. It is estimated that there are about 100,000 patients with PAH in the US, but only 15-20,000 have been diagnosed. Many others have been misdiagnosed as COPD, asthma, or congestive heart failure.
The term primary pulmonary hypertension (PPH) has now been replaced with idiopathic pulmonary arterial hypertension (IPAH) in much of the medical literature. However, some physicians continue to use the older classification inappropriately.
Familial pulmonary arterial hypertension (FPAH) and pulmonary arterial hypertension associated with anorexigens such as Fen-Phen also used to be called PPH, and now are a subcategory of PAH.

4.Diagnosis

Because pulmonary hypertension can be of five major types, a series of tests must be performed to distinguish pulmonary arterial hypertension from venous, hypoxic, thomboembolic, or miscellaneous varieties.
A physical examination is performed to look for typical signs of pulmonary hypertension. These include altered heart sounds, such as a widely split S2 or second heart sound, a loud P2 or pulmonic valve closure sound (part of the second heart sound), (para)sternal heave, possible S3 or third heart sound, and pulmonary regurgitation. Other signs include an elevated jugular venous pressure, peripheral edema (swelling of the ankles and feet), ascites (abdominal swelling due to the accumulation of fluid), hepatojugular reflux, and clubbing.
Further procedures are required to confirm the presence of pulmonary hypertension and exclude other possible diagnoses. These generally include pulmonary function tests, blood tests to exclude HIV, autoimmune diseases, and liver disease, electrocardiography (ECG), arterial blood gas measurements, X-rays of the chest (followed by high-resolution CT scanning if interstitial lung disease is suspected), and ventilation-perfusion or V/Q scanning to exclude chronic thromboembolic pulmonary hypertension. Biopsy of the lung is usually not indicated unless the pulmonary hypertension is thought to be due to an underlying interstitial lung disease. But lung biopsies are fraught with risks of bleeding due to the high intrapulmonary blood pressure. Clinical improvement is often measured by a "six-minute walk test", i.e. the distance a patient can walk in six minutes. Stability and improvement in this measurement correlate with better survival. Blood BNP level is also being used now to follow progress of patients with pulmonary hypertension.
Diagnosis of PAH requires the presence of pulmonary hypertension with two other conditions. Pulmonary artery occlusion pressure (PAOP or PCWP) must be less than 15 mm Hg (2000 Pa) and pulmonary vascular resistance (PVR) must be greater than 3 Wood units (240 dyn•s•cm-5 or 2.4 mN•s•cm-5).
Although pulmonary arterial pressure can be estimated on the basis of echocardiography, pressure measurements with a Swan-Ganz catheter provides the most definite assessment. PAOP and PVR cannot be measured directly with echocardiography. Therefore diagnosis of PAH requires right-sided cardiac catheterization. A Swan-Ganz catheter can also measure the cardiac output, which is far more important in measuring disease severity than the pulmonary arterial pressure.
Normal pulmonary arterial pressure in a person living at sea level has a mean value of 12–16 mm Hg (1600–2100 Pa). Definite pulmonary hypertension is present when mean pressures at rest exceed 25 mm Hg (3300 Pa). If mean pulmonary artery pressure rises above 30 mm Hg (4000 Pa) with exercise, that is also considered pulmonary hypertension.
Mean pulmonary artery pressure (mPAP) should not be confused with systolic pulmonary artery pressure (sPAP), which is often reported on echocardiogram reports. A systolic pressure of 40 mm Hg typically implies a mean pressure more than 25 mm Hg. Roughly, mPAP = 0.61•sPAP + 2.

3.Pathogenesis

Whatever the initial cause, pulmonary arterial hypertension (WHO Group I) involves the vasoconstriction or tightening of blood vessels connected to and within the lungs. This makes it harder for the heart to pump blood through the lungs, much as it is harder to make water flow through a narrow pipe as opposed to a wide one. Over time, the affected blood vessels become both stiffer and thicker, in a process known as fibrosis. This further increases the blood pressure within the lungs and impairs their blood flow. In addition, the increased workload of the heart causes thickening and enlargement of the right ventricle, making the heart less able to pump blood through the lungs, causing right heart failure. As the blood flowing through the lungs decreases, the left side of the heart receives less blood. This blood may also carry less oxygen than normal. Therefore it becomes harder and harder for the left side of the heart to pump to supply sufficient oxygen to the rest of the body, especially during physical activity.
Pathogenesis in pulmonary venous hypertension (WHO Group II) is completely different. There is no obstruction to blood flow in the lungs. Instead, the left heart fails to pumps blood efficiently, leading to pooling of blood in the lungs. This causes pulmonary edema and pleural effusions.
In hypoxic pulmonary hypertension (WHO Group III), the low levels of oxygen are thought to cause vasoconstriction or tightening of pulmonary arteries. This leads to a similar pathophysiology as pulmonary arterial hypertension.
In chronic thromboembolic pulmonary hypertension (WHO Group IV), the blood vessels are blocked or narrowed with blood clots. Again, this leads to a similar pathophysiology as pulmonary arterial hypertension

2.Causes

The most common cause of pulmonary hypertension is left heart failure leading to pulmonary venous hypertension (WHO Group II). This may be due to systolic or diastolic malfunction of the left ventricle or due to valvular dysfunction such as mitral regurgitation, mitral stenosis, aortic stenosis, or aortic regurgitation. It usually manifests as pulmonary edema or pleural effusions. Because the malfunctioning heart does not pump efficiently, blood fails to leave the pulmonary circulation in a timely manner, leading to abnormally high pressure in the pulmonary veins.[2] The increased pressure in the pulmonary veins can be transmitted back to the pulmonary arteries.[2]
Common causes of pulmonary arterial hypertension (PAH, WHO Group I) include HIV, scleroderma and other autoimmune disorders, cirrhosis and portal hypertension, sickle cell disease,[3] congenital heart disease, and others. Use of weight loss pills such as Fen-Phen, Aminorex, fenfluramine (Pondimin), and phentermine led to the development of PAH in the past.[4] These drugs were withdrawn from the market when the link between their use and greater incidence of PAH was established.
Human herpesvirus 8, also associated with Kaposi's sarcoma, has been demonstrated in patients with PAH, suggesting that this virus may play a role in its development.[5] Recent studies have been unable to find an association between human herpesvirus 8 and idiopathic pulmonary arterial hypertension.
When a family history exists, the disease is termed familial pulmonary arterial hypertension (FPAH). IPAH and FPAH are now considered to be genetic disorders linked to mutations in the BMPR2 gene, which encodes a receptor for bone morphogenetic proteins,[6] as well as the 5-HT(2B) gene, which codes for a serotonin receptor.[7]. There seems to be an association of idiopathic PAH (not only PAH caused by heart malformations) and Trisomy 21.
Pulmonary embolism also leads to pulmonary hypertension, acutely as well as chronically (WHO Group IV). Treatments for these two conditions are vastly different. Schistosomiasis is a very common cause of pulmonary hypertension in endemic areas such as the Nile river due to obstruction of pulmonary vessels with the parasite.
Lung diseases that lower oxygen in the blood (hypoxia) are well known causes of pulmonary hypertension (WHO Group III), including COPD, interstitial lung disease such as IPF, Pickwickian syndrome or obesity-hypoventilation syndrome, and possibly sleep apnea.
Other causes include sarcoidosis, histiocytosis X, and fibrosing mediastinitis (WHO Group V).
When none of these causes can be found, the disease is termed idiopathic pulmonary arterial hypertension (IPAH). There appears to be a link between IPAH and thyroid diseases,[8] but this is not regarded as causative.

sawasdee: Pulmonary hypertension

sawasdee: Pulmonary hypertension

1 Signs and symptoms

Signs and symptoms
A history usually reveals gradual onset of shortness of breath, fatigue, non-productive cough, angina pectoris, fainting or syncope, peripheral edema (swelling of the limbs, especially around the ankles and feet), and rarely hemoptysis (coughing up blood). Pulmonary arterial hypertension (PAH) typically does not present with orthopnea or paroxysmal nocturnal dyspnea, while pulmonary venous hypertension typically does.
In order to establish the cause, the physician will generally conduct a thorough medical history. A detailed family history is taken to determine whether the disease might be familial. A history of exposure to cocaine, methamphetamine, alcohol leading to cirrhosis, and smoking leading to emphysema are considered significant. A physical examination is performed to look for typical signs of pulmonary hypertension, including a loud P2 (pulmonic valve closure sound), (para)sternal heave, jugular venous distension, pedal edema, ascites, hepatojugular reflux, clubbing etc. Evidence of tricuspid insufficiency is also sought and, if present, is consistent with the presence of pulmonary hypertension.

Pulmonary hypertension

In medicine, pulmonary hypertension (PH) is an increase in blood pressure in the pulmonary artery, pulmonary vein, or pulmonary capillaries, together known as the lung vasculature, leading to shortness of breath, dizziness, fainting, and other symptoms, all of which are exacerbated by exertion. Depending on the cause, pulmonary hypertension can be a severe disease with a markedly decreased exercise tolerance and right-sided heart failure. It was first identified by Dr Ernst von Romberg in 1891.[1] It can be one of five different types, arterial, venous, hypoxic, thromboembolic, or miscellaneous.
Although the terms primary pulmonary hypertension (meaning of unknown cause) and secondary pulmonary hypertension (meaning due to another medical condition) still persist in materials disseminated to patients and the general public, these terms have largely been abandoned in the medical literature. This change has occurred because the older dichotomous classification did not reflect pathophysiology or outcome. It led to erroneous therapeutic decisions, i.e. treat "primary" pulmonary hypertension only. This in turn led to therapeutic nihilism for many patients labeled "secondary" pulmonary hypertension, and could have contributed to their deaths. The term "primary pulmonary hypertension" has now been replaced with "idiopathic pulmonary arterial hypertension". The terms "primary" and "secondary" pulmonary hypertension should not be used any longer. Further details are in the Classification section below.

From Wikipedia, the free encyclopedia