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Freitag, 20. Januar 2012

Oral and Maxillofacial Surgery lectures



Biopsy in oral surgeryUse SHIFT+ENTER to open the menu (new window).
Edit
bone graftUse SHIFT+ENTER to open the menu (new window).
Dento-alveolar fracturesUse SHIFT+ENTER to open the menu (new window).Edit
Differential Diagnosis of Head and SwellingUse SHIFT+ENTER to open the menu (new window).Edit
Emergency - Allergic reactionsUse SHIFT+ENTER to open the menu (new window).
Emergency Kit Part -2Use SHIFT+ENTER to open the menu (new window).Edit
Emergency-CardiacUse SHIFT+ENTER to open the menu (new window).
Emergency-EndocrineUse SHIFT+ENTER to open the menu (new window).Edit
Emergency-Respiratory emergUse SHIFT+ENTER to open the menu (new window).
Hemorrage in oral surgeryUse SHIFT+ENTER to open the menu (new window).
MALIGNANT LesionsUse SHIFT+ENTER to open the menu (new window).Edit
Management of maxillofacial traumaUse SHIFT+ENTER to open the menu (new window).Edit
Mandibular fractresUse SHIFT+ENTER to open the menu (new window).Edit
Mandibular Nerve block (Other techniques)Use SHIFT+ENTER to open the menu (new window).Edit
Mandibular Nerve blockUse SHIFT+ENTER to open the menu (new window).
Maxillary Anesthesia -1Use SHIFT+ENTER to open the menu (new window).
Maxillary Anesthesia -2Use SHIFT+ENTER to open the menu (new window).Edit
Maxillary Anesthesia -3Use SHIFT+ENTER to open the menu (new window).
Maxillary Anesthesia -4Use SHIFT+ENTER to open the menu (new window).
MaxSinus lecture 1Use SHIFT+ENTER to open the menu (new window).
MaxSinus lecture 2Use SHIFT+ENTER to open the menu (new window).
Medical emergency kit Part -1 Use SHIFT+ENTER to open the menu (new window).
Medical emergency-Medical HistoryUse SHIFT+ENTER to open the menu (new window).
Mid-face injuryUse SHIFT+ENTER to open the menu (new window).
Radical Neck DissectionUse SHIFT+ENTER to open the menu (new window).
TUMOURS OF THE HEAD AND NECKUse SHIFT+ENTER to open the menu (new window).
Unerupted and impacted IUse SHIFT+ENTER to open the menu (new window).Edit
Vascular Anomalies presentationUse SHIFT+ENTER to open the menu (new window).Edit
zygomatio-frontal FractureUse SHIFT+ENTER to open the menu (new window).

SOURCE:Dr. Hesham Khalil
BDS, MSc, OMF Prosth Certi, MFDSRCS (England), PhD

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Pulmonary hypertension


Pulmonary hypertension

From Wikipedia, the free encyclopedia
Pulmonary arterial hypertension
Classification and external resources

Micrograph showing a plexiform lesion of the lung, as seen in irreversible pulmonary hypertension. H&E stain.
ICD-10 I27.0, I27.2
ICD-9 416.0
DiseasesDB 10998
eMedicine med/1962
MeSH D006976
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. Pulmonary hypertension can be a severe disease with a markedly decreased exercise tolerance and heart failure. It was first identified by Dr. Ernst von Romberg in 1891.[1] According to the most recent classification, it can be one of five different types: arterial, venous, hypoxic, thromboembolic or miscellaneous.[2]

Contents

 [hide

[edit] Signs and symptoms

Because symptoms may develop very gradually, patients may delay seeing a physician for years. Common symptoms are shortness of breath, fatigue, non-productive cough, angina pectoris, fainting or syncope, peripheral edema (swelling around the ankles and feet), and rarely hemoptysis (coughing up blood).
Pulmonary venous hypertension typically presents with shortness of breath while lying flat or sleeping (orthopnea or paroxysmal nocturnal dyspnea), while pulmonary arterial hypertension (PAH) typically does not.
A detailed family history is established to determine whether the disease might be familial. A history of exposure to drugs such as cocaine, methamphetamine, alcohol leading to cirrhosis, and tobacco leading to emphysema are considered significant. A physical examination is performed to look for typical signs of pulmonary hypertension, including a loud S2 (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.

[edit] 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, thromboembolic, 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). Pulmonary hypertension is present when mean pulmonary artery pressure exceeds 25 mm Hg (3300 Pa) at rest or 30 mm Hg (4000 Pa) with exercise.
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 of more than 25 mm Hg. Roughly, mPAP = 0.61•sPAP + 2.

[edit] Causes and classification

A 1973 meeting organized by the World Health Organization was the first to attempt classification of pulmonary hypertension. A distinction was made between primary and secondary PH, and primary PH was divided in the "arterial plexiform", "veno-occlusive" and "thromboembolic" forms.[3] A second conference in 1998 at Évian-les-Bains also addressed the causes of secondary PH (i.e. those due to other medical conditions),[4] and in 2003, the 3rd World Symposium on Pulmonary Arterial Hypertension was convened in Venice to modify the classification based on new understandings of disease mechanisms. The revised system developed by this group provides the current framework for understanding pulmonary hypertension.[2] 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.[2]
The Venice 2003 Revised Classification system can be summarized as follows:[2]
  • WHO Group I - Pulmonary arterial hypertension (PAH)
    • Idiopathic (IPAH)
    • Familial (FPAH)
    • Associated with other diseases (APAH): collagen vascular disease (e.g. scleroderma), congenital shunts between the systemic and pulmonary circulation, portal hypertension, HIV infection, drugs, toxins, or other diseases or disorders
    • Associated with venous or capillary disease
  • 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
The classification does not include sickle cell disease,[5] 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.[6] Recent studies have been unable to find an association between human herpesvirus 8 and idiopathic pulmonary arterial hypertension.[citation needed]

[edit] 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 hypertrophy of the right ventricle, making the heart less able to pump blood through the lungs, ultimately causing right heart failure (a condition known as cor pulmonale). 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 pump 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.

[edit] Epidemiology

IPAH is a rare disease with an incidence of about 2-3 per million per year[7] and a prevalence of about 15 per million. Adult females are almost three times as likely to present with IPAH than adult males. The presentation of IPAH within children is more evenly split along gender lines.
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 (obesity-hypoventilation syndrome) is very commonly associated with right heart failure due to pulmonary hypertension.

[edit] 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.[citation needed]
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.[8] Of these, only half of the patients are responsive to calcium channel blockers in the long term.[9]
A number of agents has recently been introduced for primary and secondary PAH. The trials supporting the use of these agents have been relatively small, and the only measure consistently used to compare their effectivity is the "6 minute walk test". Many have no data on mortality benefit or time to progression.[10]

[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.
Because inexpensive generic drugs for this disease are not widely available, the World Health Organization does not include them in its model list of essential medicines.

[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) was the only inhaled form of prostacyclin approved for use in the US and Europe, until the inhaled form of treprostinil was approved by the FDA in July 2009 and is marketed under the trade name Tyvaso. The inhaled form of administration has the advantage of selective deposition in the lungs with less systemic side effects, however coughing and throat irritation commonly occur. Oral and inhaled forms of Remodulin are under development. Beraprost is an oral prostanoid available in South Korea and Japan.

[edit] Endothelin receptor antagonists

The dual (ETA and ETB) endothelin receptor antagonist bosentan (marketed as Tracleer) was approved in 2001. Sitaxentan, 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.[11] Sitaxentan has not been approved for marketing by the U.S. Food and Drug Administration (FDA). In 2010, Thelin was withdrawn by Pfizer due to severe side effects. 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.[12] 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

The U.S. FDA approved Sildenafil, a selective inhibitor of cGMP specific phosphodiesterase type 5 (PDE5), for the treatment of PAH in 2005. It is marketed for PAH as Revatio. In 2009, they also approved Tadalafil, another PDE5 inhibitor, marketed under the name Adcirca.[13]

[edit] Activators of soluble guanylate cyclase

Soluble guanylate cyclase (sGC) is the intracellular receptor for NO. As of April 2009, the sGC activators cinaciguat and riociguat are undergoing clinical trials for the treatment of PAH.

[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).
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.[14]
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.[citation needed]
Treatment regimens 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.

[edit] Monitoring

Patients are normally monitored through commonly available tests such as:
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Illinois Lemon Law

Illinois

Illinois Lemon Law

If you live in Illinois, you don't need to feel like you're stuck with a lemon. Lemon Justice has a full suite of resources that will give you useful information about Illinois new car lemons, Illinois used car lemons, as well as information about lemon trucks, lemon RVs, and lemon motorcycles.
Illinois Revised Statutes, Chapter 815, Section 380 is the state's Lemon Law.

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LEMON LAW

LEMON LAW

Things You Should Know About...LEMON LAW
Has this ever happened to you...You buy a brand new car. But instead of hitting the open road in your new "dream machine," the vehicle is spending all of its time and your money at your local auto repair shop. If so, Illinois' Lemon Law may be able to help.

Is My Vehicle a Lemon?

In order to be covered by the Illinois Lemon Law, a vehicle must:
  • have a nonconformity that both substantially impairs the use , market value or safety of the vehicle and is not repairable by the dealer or manufacturer in at least four attempts for the same repair, or
  • be out of service for a total of 30 or more business days.
The Lemon Law DOES Cover: New Cars (purchased or leased)
Light Trucks and vans under 8,000 pounds
Recreational vehicles (excluding trailers)
Vehicles in their first 12 months or 12,000 miles, whichever occurs first
Vehicles purchased in Illinois
The Lemon Law DOES NOT Cover: Used Cars
Altered or modified vehicles
Motorcycles and boats

How Does the Lemon Law Work?

Manufacturers establish an Industry Third Party Dispute Resolution Program to evaluate your claim. You can find information about this program in your vehicle ownership manual. To initiate action under the Lemon Law, contact the designated manufacturer representative for your vehicle. This representative will forward the required information and forms to you.

Preserving Your Claim

Lemon Law claims cannot be initiated directly through the dealer. Many consumers have lost their Lemon Law remedy because they waited longer than 12 months from the purchase date, the time period in which Lemon Law complaints must be filed, all the while believing they were proceeding under the Lemon Law through their dealer.
Keep in mind - it is extremely important that you file with your designated representative before your right to do so has expired!
Winning Your Claim
If the Dispute Board rules in your favor, you can expect one of the following compensations:
  • you will receive a replacement vehicle of like or similar value.
  • the manufacturer will buy your vehicle back from you, less the value for miles driven.
If you are dissatisfied with the decision of the Dispute Board, you may bring a civil action to enforce your rights under this Act. The manufacturer, however, may not dispute the board's decision.

Other Options

There are also other Federal and Illinois laws that deal with contracts and warranties for new products. Before deciding on a particular course of action, you are strongly urged to consult with a private attorney to discuss the various alternatives and determine the best course of action for your situation.

Remember- Keep Good Records!

Keep all receipts and records concerning repairs to your vehicle. Note the purpose and date of all repairs along with the length of time your vehicle is in the shop. The records you keep will be important in winning your claim!
Chicago
1-800-386-5438
TTY: 1-800-964-3013
Springfield
1-800-243-0618
TTY: 1-877-844-5461
Carbondale
1-800-243-0607
TTY: 1-877-785-9339
Printed by the authority of the state of Illinois.
This material is available in alternate format upon request.

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Pleural Mesothelioma

Pleural Mesothelioma

Malignant pleural mesotheliomaPleural Mesothelioma as compared to a healthy lung. is the most common type of mesothelioma, making up over two-thirds of all cases. Pleural mesothelioma affects the lining of the lung and chest cavity known as the pleura.
The pleura is is the membrane that surrounds the chest and lungs. This membrane, known as the mesothelium, lines several body cavities. While the pleura surrounds the lungs, cancer of the pleura is not actually lung cancer (which may also be caused by asbestos exposure).
More about the pleura and pleural mesothelioma.
Pleural mesothelioma, like all kinds of mesothelioma, can be difficult to diagnose or easily misdiagnosed. If you are aware of prior asbestos exposure, it is important to inform your physician so that mesothelioma symptoms can be correctly identified.
While a diagnosis of pleural mesothelioma is certainly serious, it is not without options. A variety of new and novel mesothelioma treatments are available, as are a variety of clinical trials.

Causes of Pleural Mesothelioma

Asbestos causes pleural mesothelioma. Used in a variety of industrial and construction applications, asbestos fibers are small, lightweight, strong, and easily airborne.
Once in the air these fibers are easily inhaled or injested, their size and sharp shape makes it easy for them work their way into the smallest passageways of the lungs and then into the pleura. Asbestos fibers thwart the body's natural defenses. Whether it is the sharp shape of the asbestos fibers, an unknown chemical reaction, or a combination of both these factors that cause the mesothelial cells of the pleura to become abnormal and divide without control is unknown. The connection, however, between asbestos and pleural mesothelioma has been clear since the begining of the 1960s.
Asbestos is the single largest cause of occupational cancer in the US1. In addition to pleural mesothelioma, asbestos causes lung cancer, other forms of mesothelioma, including peritoneal mesothelioma, and it is linked to several other types of cancer such as colon, stomach, throat, and laryngeal cancer.
In addition, absestos causes several non-cancerous conditions such as asbestosis, pleural effusions, pleural plaques, and pleural thickening (also known as pleural fibrosis). The majority of those diagnosed with these non-malignant conditions do not develop mesothelioma. However, the asbestos exposure levels associated with these conditions is an important factor to take into account when considering your risk of developing pleural mesothelioma.

Contact the Mesothelioma Center

Contact Information (Required fields are marked with an *.)
Diagnosis Have you been diagnosed with an asbestos-related disease or injury?:
  • No
  • Yes
If you answered yes, what asbestos-related disease have you been diagnosed with?:
Your Comments:

Pleural Mesothelioma Symptoms

"Do I have pleural mesothelioma?" If you have been asking yourself this question, chances are you have a history of asbestos exposure.
Pleural mesothelioma's symptoms are not specific, and may indicate other, less serious, conditions. However, if you know you have a history of asbestos exposure, it is wise to be proactive regarding your health care choices and observant of potential symptoms of pleural mesothelioma. Have regular check ups with your physician and make sure he or she is aware of your concerns and your history of asbestos exposure.
Pleural mesothelioma is a dose-dependent disease, meaning that the longer and more heavily your exposure to asbestos, the greater the chance you have of developing pleural mesothelioma (or another type of mesothelioma). This dose-dependence can also affect how quickly you are diagnosed with pleural mesothelioma, although the disease is known for its long latency periods of 10, 20, even as many as 40 years from exposure to disease progression.

Symptoms of Pleural Mesothelioma

Symptoms of pleural mesothelioma may include, but are not limited to:
Breathlessness (dyspnea)
Along with shortness of breath, patients may suffer from a cough. Rarely, patients may develop hoarsness or cough up blood (hemoptysis).
Chest pain
Chest pain is often nonspecific, and may sometimes be felt in upper abdomen, shoulder, or arm. Chest pain and breathlessness are the most common, and usually earliest presenting, symptoms of pleural mesothelioma
Weight Loss
Unexplained weight loss is cited as a symptom in about a third of pleural mesothelioma cases.
Pleural effusion
A pleural effusion is the result of too much fluid building up between the parietal and visceral pleura (linings of the chest and lungs, respectively); a pleural effusion may cause chest pain and difficulty breathing (dyspnea), however, many cause no symptoms and are first discovered during the physical examination or seen on a chest x-ray.
Night sweats
Less common, but still cited enough to be considerd a symptom of pleural mesothelioma are fever, chills, and night sweats.

Pleura Mesothelioma Diagnosis

Pleural mesothelioma, while the most common type of mesotheioma, is still a rare diagnosis. It is important that you seek out specialists who can effectively diagnose any symptoms suspected of indicating pleural mesothelioma. Many patients begin exhibiting symptoms for several months before addressing them with their physician; once in the care of a doctor, pleural mesothelioma is still somewhat tricky to diagnose, thanks to its rarity and nonspecific symptoms. While not surprising that early diagnosis is tricky, if you have a history of risk factors and concerns regarding an unusual symptoms, visit your doctor; ask about your concerns regarding pleural mesothelioma.

Diagnosing Pleural Mesothelioma

A physical exam and patient history will likely be your doctor's first step in diagnosing pleural mesothelioma. Past exposure to asbestos is a strong risk factor for pleural mesothelioma and the longer and more seriously you were exposed to asbestos, the greater your risk. If your doctor does not ask about your work history and potential mesothelioma risk factors, let him or her know about your asbestos exposure.
The next step is usually an x-ray of the chest. Pleural effusions, masses, and scarring may be seen on x-rays. Because x-rays are less sensitive than newer imaging techniques, an abnormal finding on an x-ray will likely prompt your physician to order further imaging through a CT or CAT scan or MRI. This will likely provide a better idea of the size, location, and invasiveness of the mass, but not a definitive diagnosis, nor a complete picture of if the mesothelioma has metastized into the lymph system.
Once a suspicious mass or fluid has been spotted, your doctor will probably order a thoracentesis and/or biopsy be performed.
Thoracentesis is a minimilarly invasive procedure where fluid is removed from the pleural space. As many as 95% of patients with pleural mesothelioma have pleural effusions, or excess fluid collection in the pleural space. Thoracentesis (or thoracocentesis) is generally an outpatient procedure and usually requires only local anesthestic. A hollow needle or catheter is interted into the chest to drain the accumuated fluid.
Generally the first biopsy, or tissue collection, performed is a fine-needle aspiration biopsy. Using a thin, hollow needle, cells from the suspcious mass are extracted. Like the thoracentesis, it is not as invasive as many surgical procedures and can help avoid the need for diagnostic surgery.
The collected fluid and/or biopsy tissue will then be sent for analysis by pathologist and/or cytologists. These specialists will look for signs of cancerous cells in the samples. Immunohistochemistry is the chemical staining of these samples to better identify abnormal cells. "Immunos," as these tests are sometimes called, are an important form of testing and are usually recommended.
If a definitive diagnosis has still not been reached, more invasive testing may be required. Your doctor may perform a thoracoscopy; this involves inserting a lighted scope, sometimes with a camera on it, into the chest for a closer look. If suspicious masses are seen, the doctor may cut out a sample of tissue to be examined for maligant cells.

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Peritoneal Mesothelioma (Abdominal Mesothelioma)

Peritoneal Mesothelioma (Abdominal Mesothelioma)

Malignant peritoneal mesotheliomaAbdominal cavity showing the location of the peritoneum; peritoneal mesothelioma. is an extremely rare cancer. Only 100 to 500 cases are diagnosed in the US each year, making up less than 30% of all mesothelioma cases.
Peritoneal mesothelioma is a cancer affecting the abdominal lining, or peritoneum (paira-tin-e-um), which is why is is sometimes referred to as abdominal mesothelioma. This membrane supports and covers the organs of the abdomen.
The peritoneum is made of two parts, the visceral and parietal peritoneum. The visceral peritoneum covers the internal organs and makes up most of the outer layer of the intestinal tract. Covering the abdominal cavity is the parietal peritoneum.
Cells in these linings secrete a fluid which allows organs to move against one another. For instance, as the intestines move food through the body. The cells of the mesothelium are designed to create fluid, but the cancer can cause them to overproduce, creating a build up of excess fluid in the abdominal cavity.
Because pleural mesothelioma is more common and often spreads to the peritoneal cavity, it is important to determine if pleural mesothelioma is the primary cancer.

Contact the Mesothelioma Center

Contact Information (Required fields are marked with an *.)
Diagnosis Have you been diagnosed with an asbestos-related disease or injury?:
  • No
  • Yes
If you answered yes, what asbestos-related disease have you been diagnosed with?:
Your Comments:

How does asbestos cause peritoneal mesothelioma?

Although there's no definitive explanation, it is widely believed that asbestos causes peritoneal mesothelioma in one of two ways. First, asbestos fibers may be ingested, and when in the intestinal tract, the fibers may work themselves into the peritoneal cavity and peritoneum. Second, they may be inhaled and transported through the lymph node system to the peritoneal cavity.

Peritoneal Mesothelioma Symptoms

If you are wondering "do I have peritoneal mesothelioma?" you should seek the guidance of your physician immediately; like many cancers, early detection is very important. Malignant peritoneal mesothelioma symptoms may not appear until 20 to 30 years after the first exposure to asbestos. Symptoms are usually not specific to peritoneal mesothelioma, and most often accompany other, less serious medical issues. This may make diagnosing peritoneal mesothelioma more difficult. If you have a history of asbestos exposure, your should have regular check ups with your doctor and an awareness of peritoneal mesothelioma symptoms.

Symptoms of Peritoneal Mesothelioma

Symptoms of peritoneal mesothelioma may include, but are not limited to:
Ascites
Ascites is the abnormal collection of fluid in the abdomen; when it is caused by cancer, it is referred to as malignant ascites. A cancer diagnosis is only made in about 10% of ascites cases, and of that 10%, peritoneal mesotheioma makes up only a very small percentage. Ascites can be quite uncomfortable, causing swelling of the abdomen, weight gain, indigestion, nausia, and swelling of the feet and ankles.
Pain or swelling in the abdomen
Fluid retention usually causes swelling; solid tumor masses may be responsible for pain.
Weight loss
Despite the accumulated fluid, which often increases waist size, a patient's appetite may be aversely affected by peritoneal mesothelioma resulting in weight loss.
Bowel obstruction
A blockage in the small or large intestine is a rare, and often late-occuring, symptom of peritoneal mesothelioma.
Anemia
A reduction in the number of red blood cells to below normal; this forces the heart and other organs to work harder to get oxygen where it's needed.
Fever
Infection is the most common cause of fever in cancer patients, but tumor cells can also produce fever-causing agents. A bowel obstruction may also cause fever.

Peritoneal Mesothelioma Diagnosis

Symptoms of peritoneal mesothelioma are not necessarily unique to the disease, so diagnosing peritoneal mesothelioma requires more than an observation of symptoms. Most symptoms associated with abdominal mesothelioma accompany other, often less serious, medical conditions. Most peritoneal mesothelioma diagnoses are made when the malignancy is in an advantage stage and diagnosis, alone, takes on average four months1.

Diagnosing Peritoneal Mesothelioma

The first step in diagnosing peritoneal mesothelioma is a physical exam and patient history. If your doctor does not ask about your work history and potential mesothelioma risk factors, let him or her know about your asbestos exposure. A history of asbestos exposure is an important clue for your physician or diagnostician and neglecting to mention this could delay diagnosis.
Following a physical exam and a patient's description of their symptoms, the next step in diagnosing peritoneal mesothelioma is usually to get some type of imaging of the abdomen. An x-ray, CT (or CAT) scan, or MRI may be performed. Although mesothelioma cannot be definitively diagnosed by visual confirmation, tumors may be visible, or an excess of serous fluid may be seen. The three primary types of peritoneal mesothelioma tumor development seen are:
"Dry-painful"
The most common of peritoneal mesothelioma presentations, one large or several small but similarly located peritoneal masses are seen.
"Wet"
Associated with ascites and swelling, no solid masses but small nodules and plaques are visible in this type of peritoneal mesothelioma.
"Mixed"
A combination of both "wet" and "dry" types of peritoneal mesothelioma.
In cases where fluid has accumilated in the abdomen, paracentesis may be performed; a needle is inserted into the peritoneal cavity to drain the excess fluid from the abdomen. Usually, cytologic testing on this ascetic (peritoneal) fluid (where specialists examine the fluid for abnormal cells) is not considered effective to diagnose peritoneal mesothelioma.
The next step in effectively diagnosing peritoneal mesothelioma is the collection of a biopsy. A biopsy is required so that the tissues and cells in question can be examined at a microscopic level. A fine-needle aspiration biopsy is usually performed at first because they are minorly invasive and quite safe. Immunohistochemical staining of the biopsy is regularly performed on collected samples. Sometimes referred to casually as "immunos," these tests use special substances that color proteins and markers that indicate cancerous cells.
Sometimes further testing is required to make a definitive diagnosis, whether because the initial biopsy testing was inconclusive or a fine-needle biopsy could not be taken because of the location of the tumor and/or fluid pockets. If this is the case, the next step performed is often a peritoneoscopy. During this procedure, a local anesthetic is administered and a small incision allows the doctor looks inside the abdomen with a special tool called a peritoneoscope.
During the peritoneoscopy, a larger biopsy sample may be collected for testing. Finally, if more tissue is required for testing, diagnositic surgery or "open" biopsy may be required.
Diagnosing peritoneal mesothelioma is very difficult, and cases of peritoneal mesothelioma misdiagnosed or undiagnosed are unfortunately not uncommon. It is important to share your case history of work experience (especially in shipyards and at construction sites) and asbestos exposure potential with your physicians if you feel mesothelioma is a risk. Asbestos fibres can also be carried into the home on clothing, inadvertently exposing the deadly fibres, and the risk of mesothelioma, to family members.
In addition to determing a diagnosis, many diagnostic test also help determine the stage the cancer is in, providing a better idea of a patient's prognosis. The chance of recovery depends on the size of the cancer, where the cancer is, how far the cancer has spread, how the cancer cells look under the microscope, how the cancer responds to treatment, and the patient's age. Peritoneal mesothelioma is usually diagnosed when it has had time to advance; as with most types of cancer, early diagnosis is an excellent first step in fighting the disease.

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