Pseudogout

Pseudogout

What is pseudogout?
psudogout is a type of inflammation of joints (arthritis) that is caused by deposits of crystals, called calcium pyrophosphate, in and around the joints. Pseudogout literally means "false gout."

Pseudogout has many similarities to true gout, which also can cause arthritis. However, the crystal that incites the inflammation of gout is monosodium urate. The crystals that cause pseudogout and gout each have distinct appearances when joint fluid containing them is viewed under a microscope. This makes it possible to precisely identify the cause of the joint inflammation when joint fluid is available.

Pseudogout has been reported to occasionally coexist with gout. This means that the two types crystals can sometimes be found in the same joint fluid. Researchers have also noted that the cartilage of patients who had both forms of crystals in their joint fluid was often visibly calcified, as seen on x-ray images.

What are symptoms of pseudogout?

Pseudogout can result in arthritis of a number of joints, but commonly involves the knees, wrists, shoulders, hips, and/or ankles. Pseudogout usually affects only one or a few joints at a time. The "attacks" of joint inflammation, characterized by acute joint swelling, warmth, stiffness, and pain, may last for days to weeks and can resolve spontaneously.

How does a doctor diagnose pseudogout?

Pseudogout is suggested when abnormal calcifications are seen in the cartilage of joints on x-ray testing. The arthritis of pseudogout is common in older adults, particularly in the context of dehydration such as occurs with hospitalization or surgery.

The diagnosis of pseudogout is ultimately made when fluid from a joint is examined under a special microscope called a polarizing microscope. With this microscope the calcium pyrophosphate crystals are identified.

What are treatments for pseudogout?

The treatment of pseudogout is directed toward stopping the inflammation in the joints. Local ice applications and resting can help. Nonsteroidal antiinflammatory drugs (NSAIDs), such as ibuprofen and others, are often first drugs of choice.

Removing fluid containing the crystals from the joint can reduce pain and help the inflammation to diminish more quickly. Cortisone injected into an inflamed joint, oral and intravenous colchicine are also used.

Long-term prevention of recurrent pseudogout is often best achieved with small daily doses of colchicine.

Low Blood Pressure

What is low blood pressure?

Blood pressure is the force exerted by circulating blood on the walls of blood vessels, and constitutes one of the principal vital signs. Blood pressure is generated by the heart pumping blood into the arteries and is regulated by the response by the arteries to the flow of blood.

By convention, an individual's blood pressure is expressed as systolic/diastolic blood pressure, for example, 120/80.The systolic blood pressure (the top number) represents the pressure in the arteries as the muscle of the heart contracts and pumps blood into them. The diastolic blood pressure (the bottom number) represents the pressure in the arteries as the muscle of the heart relaxes after it contracts. Blood pressure always is higher when the heart is pumping than when it is relaxing.

Systolic blood pressure for most healthy adults falls between 90 and 120 millimeters of mercury (mm Hg). Normal diastolic blood pressure falls between 60 and 80 mm Hg. Current guidelines define normal blood pressure as lower than 120/80. Blood pressures over 130/80 are considered high. High blood pressure increases the risk of developing heart disease, kidney disease, hardening of the arteries (atherosclerosis or arteriosclerosis), eye damage, and stroke.

Low blood pressure (hypotension) is pressure that is so low that it causes symptoms or signs due to the low flow of blood through the arteries and veins. When the flow of blood is too low to deliver enough oxygen and nutrients to vital organs such as the brain, heart, and kidney, the organs do not function normally and may be permanently damaged.

Unlike high blood pressure, low blood pressure is defined primarily by signs and symptoms of low blood flow not by a specific blood pressure number. Some individuals may have a blood pressure of 90/50 with no symptoms of low blood pressure and therefore do not have low blood pressure. However, others who normally have high blood pressure may develop symptoms of low blood pressure if their blood pressure drops to 100/60.

Is low blood pressure bad for your health?

People who have lower blood pressures have a lower risk of stroke, kidney disease, and heart disease. Athletes, people who exercise regularly, people who maintain ideal body weight, and non–smokers tend to have lower blood pressures. Therefore, low blood pressure is desirable as long as it is not low enough to cause symptoms and damage organs in the body.

What are low blood pressure signs and symptoms?

When the blood pressure is not sufficient to deliver enough blood to the organs of the body, the organs do not work properly and may be permanently damaged. For example, if insufficient blood flows to the brain, brain cells do not receive enough oxygen and nutrients, and a person can feel lightheaded, dizzy, or even faint. Going from a sitting or lying position to a standing position often brings out symptoms of low blood pressure. This occurs because standing causes blood to "settle" in the veins of the lower body, and this can lower the blood pressure. If the blood pressure is already low, standing can make the low pressure worse, to the point of causing symptoms. The development of lightheadedness, dizziness, or fainting upon standing caused by low blood pressure is called orthostatic hypotension. Normal individuals are able to compensate rapidly for the low pressure created by standing with the responses discussed previously and do not develop orthostatic hypotension.

When there is insufficient blood pressure to deliver blood to the coronary arteries (the arteries that supply blood to the heart's muscle), a person can develop chest pain (angina) or even a heart attack. When insufficient blood is delivered to the kidneys, the kidneys fail to eliminate wastes from the body, for example, urea and creatinine, and an increase in their levels in the blood occur (for example, elevations of blood urea nitrogen or BUN and serum creatinine, respectively).

Shock is a life–threatening condition where persistently low blood pressure causes organs such as kidney(s), liver, heart, lung, and brain to fail rapidly.

How is low blood pressure diagnosed and evaluated?

In some individuals, particularly relatively healthy ones, symptoms of weakness, dizziness, and fainting raise the suspicion of low blood pressure. In others, an event often associated with low blood pressure, for example a heart attack has occurred to cause the symptoms.

Measuring blood pressure, sometimes in both the lying (supine) and standing positions usually is the first step in diagnosing low blood pressure. In patients with symptomatic low blood pressure, there often is a marked drop in blood pressure upon standing, and patients may even develop orthostatic symptoms. The heart rate often increases greatly. Once low blood pressure has been identified as the cause of symptoms, the goal is to identify the cause of the low blood pressure. Sometimes the causes are readily apparent (such as loss of blood due to trauma, or sudden shock after receiving x–ray dyes containing iodine). At other times, the cause may be identified by testing:

CBC (complete blood count). CBC may reveal anemia from blood loss or elevated white blood cells due to infection.

Blood electrolyte measurements may show dehydration and mineral depletion, renal failure (kidney failure), or acidosis (excess acid in the blood).

Cortisol levels can be measured to diagnose adrenal insufficiency and Addison's disease.

Blood and urine cultures can be performed to diagnose septicemia and bladder infections, respectively.

Radiology studies, such as chest x–rays, abdominal ultrasounds, and computerized tomography (CT or CAT) scans may detect pneumonia, heart failure, gallstones, pancreatitis, and diverticulitis.

Electrocardiograms (EKG) can detect abnormally slow or rapid heart beats, pericarditis, and heart muscle damage from either previous heart attacks or a reduced supply of blood to the heart muscle that has not yet caused a heart attack.

Holter monitor recordings are used to diagnose intermittent episodes of abnormal heart rhythms. If abnormal rhythms occur intermittently, a standard EKG performed at the time of a visit to the doctor's office may not show the abnormal rhythm. A Holter monitor is a continuous recording of the heart's rhythm for 24 hours that often is used to diagnose intermittent episodes of bradycardia or tachycardia.

Patient–activated event recorder. If the episodes of bradycardia or tachycardia are infrequent, a 24–hour Holter recording may not capture these sporadic episodes. In this situation, a patient can wear a patient–activated event recorder for up to four weeks. The patient presses a button to start the recording when he or she senses the onset of an abnormal heart rhythm or symptoms possibly caused by low blood pressure. The doctor then analyzes the recordings at a later date to identify the abnormal episodes.

Echocardiograms are examinations of the structures and motion of the heart using ultrasound. Echocardiograms can detect pericardial fluid due to pericarditis, the extent of heart muscle damage from heart attacks, diseases of the heart valves, and rare tumors of the heart.

Ultrasound examinations of the leg veins and CT scans of the chest can detect deep vein thrombosis and pulmonary embolism.

Tilt–Table tests are used to evaluate patients suspected of having postural hypotension or syncope due to abnormal autonomic nerves. During a tilt–table test, the patient lies on an examining table with an intravenous infusion administered while the heart rate and blood pressure are monitored. The table then is tilted upright for 15 minutes to 45 minutes. Heart rate and blood pressure are monitored every few minutes. The purpose of the test is to try to reproduce postural hypotension. Sometimes a doctor may administer epinephrine (Adrenalin, Isuprel) intravenously to induce postural hypotension. For more, please read the Tilt–Table Test procedure article.

How is low blood pressure treated?

Low blood pressure in healthy subjects without symptoms or organ damage needs no treatment. However, all patients with symptoms possibly due to low blood pressure should be evaluated by a doctor. (Patients who have had a major drop in blood pressure from their usual levels even without the development of symptoms also should be evaluated.) The doctor needs to identify the cause of the low blood pressure because treatment will depend on the cause. For example, if a medication is causing the low blood pressure, the dose of medication may have to be reduced or the medication stopped, though only after consulting the doctor. Self–adjustment of medication should not be done.

Dehydration is treated with fluids and minerals (electrolytes). Mild dehydration without nausea and vomiting can be treated with oral fluids and electrolytes. Moderate to severe dehydration usually is treated in the hospital or emergency room with intravenous fluids and electrolytes.

Blood loss can be treated with intravenous fluids and blood transfusions. Continuous and severe bleeding needs to be treated immediately.

Septic shock is an emergency and is treated with intravenous fluids and antibiotics.

Blood pressure medications or diuretics are adjusted, changed, or stopped by the doctor if they are causing low blood pressure symptoms.

Bradycardia may be due to a medication. The doctor may reduce, change or stop the medication. Bradycardia due to sick sinus syndrome or heart block is treated with an implantable pacemaker.

Tachycardia is treated depending on the nature of the tachycardia. Atrial fibrillation can be treated with oral medications, electrical cardioversion, or a catheterization procedure called pulmonary vein isolation. Ventricular tachycardia can be controlled with medications or with an implantable defibrillator.

Pulmonary embolism and deep vein thrombosis is treated with blood thinners, intravenous initially with heparin, and oral warfarin (Coumadin) later.

Pericardial fluid can be removed by a procedure called pericardiocentesis.

Postural hypotension can be treated by increasing water and salt intake, using compression stockings to compress the leg veins and reduce the pooling of blood in the leg veins, and in some patients, the use of a medication called midodrine (ProAmatine). The problem with ProAmatine is that while it increases blood pressure in the upright position, the supine blood pressure may become too high, thus increasing the risk of strokes. Mayo clinic researchers found that a medication used to treat muscle weakness in Myasthenia gravis called pyridostigmine (Mestinon) increases upright blood pressure but not supine blood pressure. Mestinon is an anticholinesterase medication that works on the autonomic nervous system, especially when a person is standing up. Side effects of pyridostigmine include minor abdominal cramping or increased frequency of bowel movements. Increasing salt intake can lead to heart failure in patients with existing heart disease and should not be undertaken without consulting a doctor.

Vasovagal Syncope can be treated with several types of drugs such as beta blockers [for example, propanolol (Inderal, Inderal LA)], selective serotonin reuptake inhibitors [fluoxetine (Prozac), escitalopram oxalate (Lexapro), paroxetine (Paxil)], fludrocortisone (Florinef) (a drug that prevents dehydration by causing the kidney(s) to retaining water). A pacemaker can also be helpful when a patient fails drug therapy.

Arthritis Reumatoid

Artritis Reumatoid

Artritis rheumatoid adalah suatu penyakit inflamasi sistemik kronik dengan manifestasi utama poliartritis progresif dan melibatkan seluruh organ tubuh. Terlibatnya sendi pada pasien –pasien arthritis rheumatoid terjadi setelah penyakit ini berkembang lebih lanjut sesuai dengan progresivitasnya. Pasien dapat pula menunjukkan gejala konstitusional berupa kelemahan umum,cepat lelah, atau gangguan nonartikular lain.

KRITERIA DIAGNOSTIK ARTRITIS REUMATOID MENURUT "AMERICAN RHEUMATISM ASSOCIATION" (REVISED, 1987)

Untuk mcnegakkan diagnosis Artritis Reumatoid harus

didapati 4 atau lebih kriteria berikut ini :

1.kakupagi hari selama paling sedikit I jam dan sudah bcrlangsung paling sedikit 6 minggu.

2.epbengkakan pada 3 sendi. Terjadi pembengkakan jaringan lunak atau persendian(soft tissue swelling) atau lebih efusi, bukan pembesaran tulang (hyperostosism)

3. arthritis pada persendian tangan.

4. arthritis simetris. Maksudnya keterlibatan sendi yang sama (tidak mutlak bersifat simetris) pada kedua sisi secara serentak (symmetrical polyarthritis simultaneously )

5. Nodul reumatoidyaitu nodul subkutan pada penonjolan tulang atau permukaan ektensor atau daerah jukstaartrikular dalam obeservasi seorang dokter.

6. Faktor rheumatoid serum positif. Terdapat titer abnormal factor rheumatoid serum yang diperiksa dengan cara yang memberikan hasil positif kurang dari 5% kelompok control.

7. Terdapat perubahan gambaran radiologist yang khas pada pemeriksaan sinar roentgen tangan posteroanterior atau pergelangan tangan,yang harus menunjukkan adanya erosi atau dekalsifikasi tulang yang berlokalisasi pada sendi atau daerah yang berdekatan dengan sendi.

Patogenesis

Patogenesis penyakit ini terjadi akibat rantai peristiwa imunologikyang menyebabkan proses destruksi sendi. Berhubungan dengan factor genetic,hormonal,infeksi,dan heat shock protein. Penyakit ini lebih bayak mengenal wanita daripada pria, terutama pada usia subur.

Terapi

1. Pendidikan pada pasien mengenai penyakitnya dan penatalaksanaan yang akan dilakukan sehingga terjalin hubungan baik dan terjamin ketaatan pasien untuk tetap berobat dalam jangka waktu yang lama.

2.OAINS diberikan sejak dini untuk mengatasi nyeri sendi akibat inflamasi yang sering dijumpai

3. DMARD digunakan untuk melindungi rawan sendi dan tulang dari proses destruksi akibat arthritis rheumatoid . Mula khasiatnya baru terlihat setelah 3-12 bulan kemudian.

4. Rehabilitasi,bertujuan meningkatkan kualitas hidup pasien.Caranya antara lain dengan mengistirahatkan sendi yang terlibat,latihan,pemanasan dan lain-lain.Pengertian rehabilitasi termasuk :

a. pemakaian alat bidai,tongkat/tongkat penyangga, walking machine,kursi roda,sepatu dan alat

b. alat ortotik protetik lainnya

c. terapi mekanik

d. pemanasan: baik hidroterapi maupun elektroterapi

e. occupational therapy

5. Pembedahan

Jika berbagai cara pengobatan telah dilakukan dan tidak berhasil serta terdapat alas an yang cukup kuat , dapat dilakukan pengobatan pembedahan. Jenis pengobatan ini pada pasien arthritis rheumatoid umumnya bersifat ortopedik, misalnya sinovektomi,artrodesis,total hip replacement,memperbaiki deviasi ulnar,dlsb.

Asthma

What is asthma?

Asthma is a chronic inflammation of the bronchial tubes (airways) that causes swelling and narrowing (constriction) of the airways. The result is difficulty breathing. The bronchial narrowing is usually either totally or at least partially reversible with treatments.

Bronchial tubes that are chronically inflamed may become overly sensitive to allergens (specific triggers) or irritants (nonspecific triggers). The airways may become "twitchy" and remain in a state of heightened sensitivity. This is called "Bronchial Hyperreactivity" (BHR). It is likely that there is a spectrum of bronchial hyperreactivity in all individuals. However, it is clear that asthmatics and allergic individuals (without apparent asthma) have a greater degree of bronchial hyperreactivity than non-asthmatic and nonallergic people. In sensitive individuals, the bronchial tubes are more likely to swell and constrict when exposed to triggers such as allergens, tobacco smoke, or exercise. Amongst asthmatics, some may have mild BHR and no symptoms while others may have severe BHR and chronic symptoms.

Asthma affects people differently. Each individual is unique in their degree of reactivity to environmental triggers. This naturally influences the type and dose of medication prescribed, which may vary from one individual to another.

How does asthma affect breathing?

Asthma causes a narrowing of the breathing airways, which interferes with the normal movement of air in and out of the lungs. Asthma involves only the bronchial tubes and does not affect the air sacs or the lung tissue. The narrowing that occurs in asthma is caused by three major factors: inflammation, bronchospasm, and hyperreactivity.

Inflammation
The first and most important factor causing narrowing of the bronchial tubes is inflammation. The bronchial tubes become red, irritated, and swollen. The inflammation occurs in response to an allergen or irritant and results from the action of chemical mediators (histamine, leukotrienes, and others). The inflamed tissues produce an excess amount of "sticky" mucus into the tubes. The mucus can clump together and form "plugs" that can clog the smaller airways. Specialized allergy and inflammation cells (eosinophils and white blood cells), which accumulate at the site, cause tissue damage. These damaged cells are shed into the airways, thereby contributing to the narrowing.

Bronchospasm

The muscles around the bronchial tubes tighten during an attack of asthma. This muscle constriction of the airways is called bronchospasm. Bronchospasm causes the airway to narrow further. Chemical mediators and nerves in the bronchial tubes cause the muscles to constrict.

Hyperreactivity (Hypersensitivity)

In patients with asthma, the chronically inflamed and constricted airways become highly sensitive, or reactive, to triggers such as allergens, irritants, and infections. Exposure to these triggers may result in progressively more inflammation and narrowing.

The combination of these three factors results in difficulty with breathing out, or exhaling. As a result, the air needs to be forcefully exhaled to overcome the narrowing, thereby causing the typical "wheezing" sound. People with asthma also frequently "cough" in an attempt to expel the thick mucus plugs. Reducing the flow of air may result in less oxygen passing into the bloodstream and if very severe, carbon dioxide may dangerously accumulate in the blood.

Types: allergic (extrinsic) and nonallergic (intrinsic) asthma

Your doctor may refer to asthma as being "extrinsic" or "intrinsic." A better understanding of the nature of asthma can help explain the differences between them. Extrinsic, or allergic asthma, is more common (90% of all cases) and typically develops in childhood. Approximately 80% of children with asthma also have documented allergies. Typically, there is a family history of allergies. Additionally, other allergic conditions, such as nasal allergies or eczema, are often also present. Allergic asthma often goes into remission in early adulthood. However, in 75% of cases, the asthma reappears later.

Intrinsic asthma represents about 10% of all cases. It usually develops after the age of 30 and is not typically associated with allergies. Women are more frequently involved and many cases seem to follow a respiratory tract infection. The condition can be difficult to treat and symptoms are often chronic and year-round.

Typical symptoms and signs of asthma

The symptoms of asthma vary from person to person and in any individual from time to time. It is important to remember that many of these symptoms can be subtle and similar to those seen in other conditions. All of the symptoms mentioned below can be present in other respiratory, and sometimes, in heart conditions. This potential confusion makes identifying the settings in which the symptoms occur and diagnostic testing very important in recognizing this disorder.

The Four Major Recognized Symptoms:

Shortness of breath - especially with exertion or at night

Wheezing - a whistling or hissing sound when breathing out

Coughing - may be chronic; usually worse at night and early morning; and may occur after exercise or when exposed to cold, dry air

Chest tightness - may occur with or without the above symptoms

Asthma is classified according to the frequency and severity of symptoms, or "attacks," and the results of pulmonary (lung) function tests.

30% of affected patients have mild, intermittent (less than two episodes a week) symptoms of asthma with normal breathing tests

30% have mild, persistent (two or mores episodes a week) symptoms of asthma with normal or abnormal breathing tests

40% have moderate or severe, persistent (daily or continuous) symptoms of asthma with abnormal breathing tests

Acute asthma attack

An acute, or sudden, asthma attack is usually caused by an exposure to allergens or an upper respiratory tract infection. The severity of the attack depends on how well your underlying asthma is being controlled (reflecting how well the airway inflammation is being controlled). An acute attack is potentially life-threatening because it may continue despite the use of your usual quick-relief medications (inhaled bronchodilators). Asthma that is unresponsive to treatment with an inhaler should prompt you to seek medical attention at the closest hospital emergency room or your asthma specialist office, depending on the circumstances and time of day. Asthma attacks do not stop on their own without treatment. If you ignore the early warning signs, you put yourself at risk of developing "status asthmaticus."

The symptoms of severe asthma are persistent coughing and the inability to speak full sentences or walk without shortness of breath. Your chest may feel closed and your lips may have a bluish tint. In addition, you may feel agitation, confusion, or an inability to concentrate. You may hunch your shoulders, sit or stand up to breathe more easily, and strain your abdominal and neck muscles. These are signs of an impending respiratory system failure. At this point, it is unlikely that inhaled medications will reverse this process. A mechanical ventilator may be needed to assist the lungs and respiratory muscles. A face mask or a breathing tube is inserted in the nose or mouth for this treatment. These breathing aids are temporary and are removed once the attack has subsided and the lungs have recovered sufficiently to resume the work of breathing on their own. A short hospital stay in an intensive care unit may be a result of a severe attack that has not been promptly treated. To avoid such hospitalization, it is best, at the onset of symptoms, to begin immediate early treatment at home or in your doctor's office.

. What medication are used for treatment?

Most asthma medications work by relaxing bronchospasm (bronchodilators) or reducing inflammation (corticosteroids). In the treatment of asthma, inhaled medications are generally preferred over tablet or liquid medicines which are swallowed (oral medications). Inhaled medications act directly on the airway surface and airway muscles where the asthma problems initiate. Absorption of inhaled medications into the rest of the body is minimal. Therefore, adverse side effects are fewer as compared to oral medications. Inhaled medications include beta-2 agonists, anticholinergics, corticosteroids, and cromolyn sodium. Oral medications include aminophylline, leukotriene antagonists, and corticosteroid tablets.

Historically, one of the first medications used for asthma was adrenaline (epinephrine). Adrenaline has a rapid onset of action in opening the airways (bronchodilation). It is still often used in emergency situations for asthma. Unfortunately, adrenaline has many side effects, including rapid heart rate, headache, nausea, vomiting, restlessness, and a sense of panic.

Medications chemically similar to adrenaline have been developed. These medications, called beta-2 agonists, have the bronchodilating benefits of adrenaline without many of its unwanted side-effects. Beta-2 agonists are inhaled bronchodilators which are called "agonists" because they promote the action of the beta-2 receptor of bronchial wall muscle. This receptor acts to relax the muscular wall of the airways (bronchi), resulting in bronchodilation. The bronchodilator action of beta- 2 agonists starts within minutes after inhalation and lasts for about four hours. Examples of these medications include albuterol (Ventolin, Proventil), metaproterenol (Alupent), pirbuterol acetate (Maxair), and terbutaline sulfate (Brethaire).

A new group of long-acting beta-2 agonists has been developed with a sustained duration of effect of 12 hours. These inhalers can be taken twice a day. Salmeterol xinafoate (Serevent) is an example of this group of medications. The long-acting beta-2 agonists are generally not used for acute attacks. Beta-2 agonists can have side effects, such as anxiety, tremor, palpitations or fast heart rate, and lowering of blood potassium.

Just as beta-2 agonists can dilate the airways, beta blocker medications impair the relaxation of bronchial muscle by beta-2 receptors and can cause constriction of airways, aggravating asthma. Therefore, beta blockers, such as the blood pressure medications propanolol (Inderal), and atenolol (Tenormin), should be avoided by asthma patients if possible.

The anticholinergic agents act on a different type of nerves than the beta-2 agonists to achieve a similar relaxation and opening of the airway passages. These two groups of bronchodilator inhalers when used together can produce an enhanced bronchodilation effect. An example of a commonly used anticholinergic agent is ipratropium bromide (Atrovent). Ipratropium takes longer to work as compared with the beta-2 agonists, with peak effectiveness occurring two hours after intake and lasting six hours. Anticholinergic agents can also be very helpful medications for patients with emphysema.

When symptoms of asthma are difficult to control with beta-2 agonists, inhaled corticosteroids (cortisone) are often added. Corticosteroids can improve lung function and reduce airway obstruction over time. Examples of inhaled corticosteroids include beclomethasone dipropionate (Beclovent, Beconase, Vancenase, and Vanceril), triamcinolone acetonide (Azmacort), and flunisolide (Aerobid). The ideal dose of corticosteroids is still unknown. The side effects of inhaled corticosteroids include hoarseness, loss of voice, and oral yeast infections. Early use of inhaled corticosteroids may prevent irreversible damage to the airways.

Cromolyn sodium (Intal) prevents the release of certain chemicals in the lungs, such as histamine, which can cause asthma. Exactly how cromolyn works to prevent asthma needs further research. Cromolyn is not a corticosteroid and is usually not associated with significant side effects. Cromolyn is useful in preventing asthma but has limited effectiveness once acute asthma starts. Cromolyn can help prevent asthma triggered by exercise, cold air, and allergic substances, such as cat dander. Cromolyn may be used in children as well as adults.

Theophylline (Theodur, Theoair, Slo-bid, Uniphyl, Theo-24) and aminophylline are examples of methylxanthines. Methylxanthines are administered orally or intravenously. Before the inhalers became popular, methylxanthines were the mainstay of treatment of asthma. Caffeine that is in common coffee and soft drinks is also a methylxanthine drug! Theophylline relaxes the muscles surrounding the air passages and prevents certain cells lining the bronchi (mast cells) from releasing chemicals, such as histamine, which can cause asthma. Theophylline can also act as a mild diuretic, causing an increase in urination. For asthma that is difficult to control, methylxanthines can still play an important role. Dosage levels of theophylline or aminophylline are closely monitored. Excessive levels can lead to nausea, vomiting, heart rhythm problems, and even seizures. In certain medical conditions, such as heart failure or cirrhosis, dosages of methylxanthines are lowered to avoid excessive blood levels. Drug interactions with other medications, such as cimetidine (Tagamet), calcium channel blockers (Procardia), quinolones (Cipro), and allopurinol (Xyloprim) can further affect drug blood levels.

Corticosteroids are given orally for severe asthma unresponsive to other medications. Unfortunately, high doses of corticosteroids over long periods can have serious side effects, including osteoporosis, bone fractures, diabetes mellitus, high blood pressure, thinning of the skin and easy bruising, insomnia, emotional changes, and weight gain.

Expectorants help thin airway mucus, making it easier to clear the mucus by coughing. Potassium iodide is not commonly used and has the potential side-effects of acne, increased salivation, hives, and thyroid problems. Guaifenesin (Entex, Humibid) can increase the production of fluid in the lungs and help thin the mucus, but can also be an airway irritant for some people.

In addition to bronchodilator medications for those patients with atopic asthma, avoiding allergens or other irritants can be very important. In patients who cannot avoid the allergens, or in those whose symptoms cannot be controlled by medications, allergy shots are considered. The benefits of allergy shots (desensitization) in the prevention of asthma has not been firmly established. Some doctors are still concerned about the risk of anaphylaxis, which occurs in one in 2 million doses given. Allergy shots most commonly benefit children allergic to house dust mites. Other benefits can be seen with pollens and animal dander.

In some asthma patients, avoidance of aspirin, or other NSAIDs (commonly used in treating arthritis inflammation) is important. In other patients, adequate treatment of backflow of stomach acid (esophageal reflux) prevents irritation of the airways. Measures to prevent esophageal reflux include medications, weight loss, dietary changes, and stopping cigarettes, coffee, and alcohol. Examples of medications used to reduce reflux include omeprazole (Prilosec) and ranitidine (Zantac). Patients with severe reflux problems causing lung problems may need surgery to strengthen the esophageal sphincter in order to prevent acid reflux (fundoplication surgery).

Osteoartritis

OSTEOARTRITIS

Osteoartritis disebut juga penyakit sendi degeneratif atau arthritis hipertrofi.Penyakit ini merupakan penyakit kerusakan tulang rawan yang bekembang lambat dan berhubungan dengan usia lanjut. Secara klinis ditandai dengan nyeri,deformitas,pembesaran sendi dan hambatan gerak pada sendi-sendi tangan dan sendi besar yang menanggung beban.Sering kali berhubungan dengan trauma atau mikrotruma yang berulang-ulang,obesitas,stress oleh beban tubuh, dan penyakit sendi – sendi lainnya.

Etiologi

Etiologi penyakit ini tidak diketahui dengan pasti.ada beberapa factor resiko yang diketahui berhubungan dengan penyakit ini, yaitu:

1. usia lebih dari 40 tahun
2. jenis kelamin,wanita lebih sering
3. suku bangsa
4. genetic
5. kegemukan dan penyakit metabolic
6. cedera sendi,pekerjaan dan olahraga
7. kelainan pertumbuhan
8. kepadatan tulang , dll

Apa gejala dari osteoarthritis??

Gejala pada osteoarthritis timbul secara bertahap. Awalnya kelainan berupa nyeri dan kekakuan pada sendi. Sendi-sendi jari tangan, pangkal ibu jari, leher, punggung sebelah bawah, jari kaki yang besar, panggul dan lutut adalah bagian yang paling sering terkena osteoartritis. Nyeri dapat bersifat ringan, sedang, atau berat hingga dapat mengganggu aktivitas sehari-hari. Bila penyakit berlanjut maka makin lama sendi akan makin sulit untuk digerakkan dan pada akhirnya akan terhenti pada posisi tertekuk.

Pertumbuhan baru dari tulang rawan dan jaringan lainya dapat menyebabkan membesarnya sendi, dan tulang rawan yang permukaanya kasar akan menyebabkan timbulnya suara gemeretak pada saat sendi digerakkan. Pada beberapa sendi, ligamen (yang mengelilingi dan menyokong sendi) dapat teregang sehingga sendi menjadi tidak stabil. Menyentuh atau menggerakkan sendi ini bisa menyebabkan nyeri yang hebat.

Osteoartritis yang terjadi pada sendi-sendi di leher atau punggung dapat menimbulkan gejala mati rasa, kesemutan, nyeri dan kelemahan pada lengan atau tungkai, jika pertumbuhan tulang berlebihan menekan persarafan yang ada di sekitarnya. Kadang dapat terjadi penekanan pada pembuluh darah yang menuju ke otak bagian belakang, sehingga dapat timbul gangguan pengelihatan, vertigo, mual dan muntah. Pertumbuhan tulang yang terjadi di sekitar leher juga dapat menyebakan gangguan pada proses menelan

Bagaimana Mendiagnosis Osteoartritis?

Diagnosis dari osteoartritis dapat ditegakan berdasarkan gejala penyakit dan dengan melakukan pemeriksaan tambahan. Pemeriksaan tambahan yang dimaksud dapat berupa :

1. Röntgen tulang

Dengan pemeriksaan ini dapat diketahui kerusakan atau perubahan-perubahan yang terjadi pada tulang rawan atau tulang yang mengindikasikan adanya osteoartritis.

2. MRI (Magnetic Resonance Imaging)

Pada MRI dapat pula dilihat kelainan-kelainan yang terjadi pada tulang rawan dan tulang dengan detail yang lebih baik daripada pemeriksaan röntgen tulang.

3. Aspirasi sendi (arthrocentesis)

Pemeriksaan ini dilakukan dengan cara mengambil sedikit cairan yang ada di dalam sendi untuk diperiksa di laboratorium berkenaan dengan adanya kelainan pada sendi.

Terapi Osteoartritis

Sampai saat ini masih belum ditemukan obat yang dapat menyembuhkan osteoartritis hingga tuntas. Pengobatan yang ada hingga saat ini hanya berfungsi untuk mengurangi nyeri dan mempertahankan fungsi dari sendi yang terkena. Ada tiga tujuan utama yang ingin dicapai dalam proses terapi osteoartritis, yaitu untuk mengontrol nyeri dan gejala lainya, untuk mengatasi gangguan pada aktivitas sehari-hari, dan untuk menghambat proses penyakit.

Pilihan pengobatan dapat olahraga, kontrol berat badan, perlindungan sendi, terapi fisik, dan obat-obatan. Bila semua pilihan terapi tersebut tidak memberikan hasil, dapat dipertimbangkan untuk dilakukan tindakan operasi pada sendi yang terkena.

Glucosamine dan Chondroitin Sulfate

Glucosamine merupakan suatu gula amino yang berfungsi untuk pembentukan dan perbaikan kartilago. Chondroitin sulfate merupakan bagian dari molekul protein besar (proteoglycan) yang memberikan elastisitas dari kartilago. Studi menunjukkan bahwa penderita osteoartritis yang mengonsumsi suplemen glucosamine dan chondroitin sulfate mengalami pengurangan rasa nyeri dalam intensitas yang sama seperti bila seseorang mengonsumsi obat AINS (Anti Inflamasi Non-Steroid). Selain itu kedua zat tersebut juga dipercaya dapat memperlambat kerusakan kartilago pada pederita osteoartritis.

High Blood Pressure

High Blood Pressure

High blood pressure (hbp) or hypertension means high pressure (tension) in the arteries. Arteries are vessels that carry blood from the pumping heart to all the tissues and organs of the body. High blood pressure does not mean excessive emotional tension, although emotional tension and stress can temporarily increase blood pressure. Normal blood pressure is below 120/80; blood pressure between 120/80 and 139/89 is called "pre–hypertension", and a blood pressure of 140/90 or above is considered high.

The top number, the systolic blood pressure, corresponds to the pressure in the arteries as the heart contracts and pumps blood forward into the arteries. The bottom number, the diastolic pressure, represents the pressure in the arteries as the heart relaxes after the contraction. The diastolic pressure reflects the lowest pressure to which the arteries are exposed.

An elevation of the systolic and/or diastolic blood pressure increases the risk of developing heart (cardiac) disease, kidney (renal) disease, hardening of the arteries (atherosclerosis or arteriosclerosis), eye damage, and stroke (brain damage). These complications of hypertension are often referred to as end–organ damage because damage to these organs is the end result of chronic (long duration) high blood pressure. For that reason, the diagnosis of high blood pressure is important so efforts can be made to normalize blood pressure and prevent complications.

It was previously thought that rises in diastolic blood pressure were a more important risk factor than systolic elevations, but it is now known that in people 50 years or older systolic hypertension represents a greater risk.

Affecting approximately one in four adults in the United States, hypertension is clearly a major public health problem.

What causes high blood pressure?

Two forms of high blood pressure have been described: essential (or primary) hypertension and secondary hypertension. Essential hypertension is a far more common condition and accounts for 95% of hypertension. The cause of essential hypertension is multifactorial, that is, there are several factors whose combined effects produce hypertension. In secondary hypertension, which accounts for 5% of hypertension, the high blood pressure is secondary to (caused by) a specific abnormality in one of the organs or systems of the body. (Secondary hypertension is discussed further in a separate section below.)

Essential hypertension affects approximately 75 million Americans, yet its basic causes or underlying defects are not always known. Nevertheless, certain associations have been recognized in people with essential hypertension. For example, essential hypertension develops only in groups or societies that have a fairly high intake of salt, exceeding 5.8 grams daily. In fact, salt intake may be a particularly important factor in relation to essential hypertension in several situations. Thus, excess salt may be involved in the hypertension that is associated with advancing age, African American background, obesity, hereditary (genetic) susceptibility, and kidney failure (renal insufficiency).

Genetic factors are thought to play a prominent role in the development of essential hypertension. However, the genes for hypertension have not yet been identified. (Genes are tiny portions of chromosomes that produce the proteins that determine the characteristics of individuals.) The current research in this area is focused on the genetic factors that affect the renin–angiotensin–aldosterone system. This system helps to regulate blood pressure by controlling salt balance and the tone (state of elasticity) of the arteries.

Approximately 30% of cases of essential hypertension are attributable to genetic factors. For example, in the United States, the incidence of high blood pressure is greater among African Americans than among Caucasians or Asians. Also, in individuals who have one or two parents with hypertension, high blood pressure is twice as common as in the general population. Rarely, certain unusual genetic disorders affecting the hormones of the adrenal glands may lead to hypertension. (These identified genetic disorders are actually considered secondary hypertension.)

The vast majority of patients with essential hypertension have in common a particular abnormality of the arteries: an increased resistance (stiffness or lack of elasticity) in the tiny arteries that are most distant from the heart (peripheral arteries or arterioles). The arterioles supply oxygen–containing blood and nutrients to all of the tissues of the body. The arterioles are connected by capillaries in the tissues to the veins (the venous system), which returns the blood to the heart and lungs. Just what makes the peripheral arteries become stiff is not known. Yet, this increased peripheral arteriolar stiffness is present in those individuals whose essential hypertension is associated with genetic factors, obesity, lack of exercise, overuse of salt, and aging. Inflammation also may play a role in hypertension since a predictor of the development of hypertension is the presence of an elevated C reactive protein level (a blood test marker of inflammation) in some individuals.

What do patients feel with high blood pressure?

Uncomplicated high blood pressure usually occurs without any symptoms (silently) and so hypertension has been labeled "the silent killer." It is called this because the disease can progress to finally develop any one or more of the several potentially fatal complications of hypertension such as heart attacks or strokes. Uncomplicated hypertension may be present and remain unnoticed for many years, or even decades. This happens when there are no symptoms, and those affected fail to undergo periodic blood pressure screening.

Some people with uncomplicated hypertension, however, may experience symptoms such as headache, dizziness, shortness of breath, and blurred vision. The presence of symptoms can be a good thing in that they can prompt people to consult a doctor for treatment and make them more compliant in taking their medications. Often, however, a person's first contact with a physician may be after significant damage to the end–organs has occurred. In many cases, a person visits or is brought to the doctor or an emergency room with a heart attack, stroke, kidney failure, or impaired vision (due to damage to the back part of the retina). Greater public awareness and frequent blood pressure screening may help to identify patients with undiagnosed high blood pressure before significant complications have developed.

About one out of every 100 (1%) people with hypertension is diagnosed with severe high blood pressure (accelerated or malignant hypertension) at their first visit to the doctor. In these patients, the diastolic blood pressure (the minimum pressure) exceeds 140 mm Hg! Affected persons often experience severe headache, nausea, visual symptoms, dizziness, and sometimes kidney failure. Malignant hypertension is a medical emergency and requires urgent treatment to prevent a stroke (brain damage).

Artritis Gout

Artritis Gout

Seseorang dikatakan menderita asam urat (gout) jika kondisinya memenuhi beberapa syarat dan biasanya perjalanan penyakitnya klasik sekali, seperti mempunyai gejala yang khas penyakit gout, mempunyai perjalanan yang khas penyakit gout, ditemukan asam urat dalam kadar tinggi dalam darahnya, dan hasil pemeriksaan mikroskopik dari cairan sendi atau tofus (benjolan asam urat) ditemukan kristal asam urat yang berbentuk jarum.

Umumnya yang terserang asam urat adalah para pria, sedangkan pada perempuan presentasinya kecil dan baru muncul setelah menopause.

Mengapa asam urat cenderung dialami pria? Ini karena perempuan mempunyai hormon estrogen yang ikut membantu pembuangan asam urat lewat urine. Sementara pada pria, asam uratnya cenderung lebih tinggi daripada perempuan karena tidak memiliki hormon estrogen tersebut.

Jadi, selama seorang perempuan mempunyai hormon estrogen, maka pembuangan asam uratnya ikut terkontrol. Ketika sudah tidak mempunyai estrogen, seperti saat menopause, barulah perempuan terkena asam urat. Dengan kata lain, asam urat bisa disebut sebagai penyakit kaum pria.

Kadar asam urat

Kadar asam urat normal pada pria berkisar 3,5-7 mg/dl dan pada perempuan 2,6-6 mg/dl. Kadar asam urat di atas normal disebut hiperurisemia. Perjalanan penyakit yang klasik biasanya dimulai dengan suatu serangan atau seseorang memiliki riwayat pernah cek asam uratnya tinggi di atas 7 mg/dl, dan makin lama makin tinggi.

Jika demikian, kemungkinannya untuk menjadi penyakit gout itu makin besar. Biasanya 25 persen orang yang asam uratnya tinggi akan menjadi penyakit gout. Itu disebut awal stadium, asimtomatik, tanpa gejala. Pada setiap orang berbeda-beda. Ada yang bertahun-tahun sama sekali tidak muncul gejalanya, tetapi ada yang muncul gejalanya di usia 20 tahun, 30 tahun, atau 40 tahun.

Serangan “gout” terjadi tanpa diperkirakan atau mendadak dan kebanyakan menyerang pada malam hari. Biasanya, munculnya gout ditandai dengan adanya serangan berulang pada peradangan sendi yang akut, juga ditemukan pembentukan kristal natrium urat besar yang dinamakan tophus, adanya kerusakan sendi secara kronis, dan cedera pada ginjal

Artristis gout muncul sebagai serangan keradangan sendi yang timbul berulang-ulang. Gejala khas dari serangan artritis gout adalah pembengkakan, kemerahan, nyeri hebat, panas dan gangguan gerak dari sendi yang terserang yang terjadi mendadak (akut) yang mencapai puncaknya kurang dari 24 jam.

Perjalanan penyakit gout sangat khas dan mempunyai tiga tahapan. Tahap pertama disebut tahap artritis gout akut. Pada tahap ini penderita akan mengalami serangan artritis yang khas dan serangan tersebut akan menghilang tanpa pengobatan dalam waktu 5-7 hari. Karena cepat menghilang, maka sering penderita menduga kakinya keseleo atau kena infeksi sehingga tidak menduga terkena penyakit gout dan tidak melakukan pemeriksaan lanjutan.

Bahkan, dokter yang mengobati kadang-kadang tidak menduga penderita terserang penyakit gout. Karena serangan pertama kali ini singkat waktunya dan sembuh sendiri, sering penderita berobat ke tukang urut dan waktu sembuh menyangka hal itu disebabkan hasil urutan/pijatan. Padahal, tanpa diobati atau diurut pun serangan pertama kali ini akan hilang sendiri.

Setelah serangan pertama, penderita akan masuk pada gout interkritikal. Pada keadaan ini penderita dalam keadaan sehat selama jangka waktu tertentu. Jangka waktu antara seseorang dan orang lainnya berbeda. Ada yang hanya satu tahun, ada pula yang sampai 10 tahun, tetapi rata-rata berkisar 1-2 tahun. Panjangnya jangka waktu tahap ini menyebabkan seseorang lupa bahwa ia pernah menderita serangan artritis gout akut atau menyangka serangan pertama kali dahulu tak ada hubungannya dengan penyakit gout.

Tahap kedua disebut sebagai tahap artritis gout akut intemiten. Setelah melewati masa gout interkritikal selama bertahun-tahun tanpa gejala, penderita akan memasuki tahap ini, ditandai dengan serangan artritis yang khas. Selanjutnya penderita akan sering mendapat serangan (kambuh) yang jarak antara serangan yang satu dan serangan berikutnya makin lama makin rapat dan lama, serangan makin lama makin panjang, serta jumlah sendi yang terserang makin banyak.

Tahap ketiga disebut sebagai tahap artritis gout kronik bertofus. Tahap ini terjadi bila penderita telah menderita sakit selama 10 tahun atau lebih. Pada tahap ini akan terjadi benjolan-benjolan di sekitar sendi yang sering meradang yang disebut sebagai tofus. Tofus ini berupa benjolan keras yang berisi serbuk seperti kapur yang merupakan deposit dari kristal monosodium urat. Tofus ini akan mengakibatkan kerusakan pada sendi dan tulang di sekitarnya. Tofus pada kaki bila ukurannya besar dan banyak akan mengakibatkan penderita tidak dapat menggunakan sepatu lagi.

Faktor risiko

faktor risiko yang menyebabkan orang terserang penyakit asam urat adalah pola makan, kegemukan, dan suku bangsa. Asupan yang masuk ke tubuh juga memengaruhi kadar asam urat dalam darah. Makanan yang mengandung zat purin yang tinggi akan diubah menjadi asam urat. Purin yang tinggi terutama terdapat dalam jeroan, sea food: udang, cumi, kerang, kepiting, ikan teri.

Yang paling penting untuk diketahui adalah kalau asam urat tinggi dalam darah, tanpa kita sadari akan merusak organ-organ tubuh, terutama ginjal, karena saringannya akan tersumbat. Tersumbatnya saringan ginjal akan berdampak munculnya batu ginjal, atau akhirnya bisa mengakibatkan gagal ginjal.

Asam urat pun merupakan faktor risiko untuk penyakit jantung koroner. Diduga kristal asam urat akan merusak endotel/pembuluh darah koroner

Serangan gout (artritis gout akut) terjadi secara mendadak. Timbulnya serangan bisa dipicu oleh:

luka ringan

pembedahan

pemakaian sejumlah besar alkohol atau makanan yang kaya akan protein

kelelahan

stres emosional

penyakit.

Pengobatan

Langkah pertama untuk mengurangi nyeri adalah mengendalikan peradangan. Pengobatan tradisional untuk gout adalah kolkisin. Biasanya nyeri sendi mulai berkurang dalam waktu 12-24 jam setelah pemberian kolkisin dan akan menghilang dalam waktu 48-72 jam. Kolkisin diberikan dalam bentuk tablet, tetapi jika menyebabkan gangguan pencernaan, bisa diberikan secara intravena. Obat ini seringkali menyebabkan diare dan bisa menyebabkan efek samping yang lebih serius (termasuk kerusakan sumsum tulang).

Saat ini obat anti peradangan non-steroid (misalnya ibuprofen dan indometasin) lebih banyak digunakan daripada kolkisin dan sangat efektif mengurangi nyeri dan pembengkakan sendi. Kadang diberikan kortikosteroid (misalnya prednison). Jika penyakit ini mengenai 1-2 sendi, suatu larutan kristal kortikosteroid bisa disuntikkan langsung ke dalam sendi. Pengobatan ini sangat efektif untuk mengakhiri peradangan yang disebabkan oleh kristal urat.

Kadang obat pereda nyeri ditambahkan untuk mengendalikan nyeri (misalnya kodein dan meperidin). Untuk mengurangi nyeri, sendi yang meradang sebaiknya diistirahatkan dahulu.

Obat-obat seperti probenesid atau sulfinpirazon berfungsi menurunkan kadar asam urat dalam darah dengan jalan meningkatkan pembuangan asam urat ke dalam air kemih. Aspirin menghambat efek probenesid dan sulfinpirazon, sehingga sebaiknya tidak digunakan pada saat yang bersamaan. Jika diperlukan obat pereda nyeri, lebih baik diberikan asetaminofen atau obat anti peradangan non-steroid (misalnya ibuprofen).

Jika pembuangan asam urat meningkat, dianjurkan untuk minum banyak air (minimal 2 liter/hari) untuk membantu mengurangi resiko kerusakan sendi dan ginjal.

Allopurinol merupakan obat yang menghambat pembentukan asam urat di dalam tubuh. Obat ini terutama diberikan kepada penderita yang memiliki kadar asam urat yang tinggi dan batu ginjal atau mengalami kerusakan ginjal. Allopurinol bisa menyebabkan gangguan pencernaan, timbulnya ruam di kulit, berkurangnya jumlah sel darah putih dan kerusakan hati.

Sebagian besar tofi di telinga, tangan atau kaki akan mengecil secara perlahan jika kadar asam urat dalam darah berkurang; tetapi tofi yang sangat besar mungkin harus diangkat melalui pembedahan.

Orang yang memiliki kadar asam urat yang tinggi tetapi tidak menunjukkan gejala-gejala gout, kadang mendapatkan obat untuk menurunkan kadar asam uratnya. Tetapi karena adanya efek samping dari obat tersebut, maka pemakaiannya ditunda kecuali jika kadar asam urat di dalam air kemihnya sangat tinggi. Pemberian allopurinol bisa mencegah pembentukan batu ginjal.

Pencegahan

Penyakitnya sendiri tidak bisa dicegah, tetapi beberapa faktor pencetusnya bisa dihindari (misalnya cedera, alkohol, makanan kaya protein).

Untuk mencegah kekambuhan, dianjurkan untuk minum banyak air, menghindari minuman beralkohol dan mengurangi makanan yang kaya akan protein. Banyak penderita yang memiliki kelebihan berat badan, jika berat badan mereka dikurangi, maka kadar asam urat dalam darah seringkali kembali ke normal atau mendekati normal.

Beberapa penderita (terutama yang mengalami serangan berulang yang hebat) mulai menjalani pengobatan jangka panjang pada saat gejala telah menghilang dan pengobatan dilanjutkan sampai diantara serangan. Kolkisin dosis rendah diminum setiap hari dan bisa mencegah serangan atau paling tidak mengurangi frekuensi serangan. Mengkonsumsi obat anti peradangan non-steroid secara rutin juga bisa mencegah terjadinya serangan. Kadang kolkisin dan obat anti peradangan non-steroid diberikan dalam waktu yang bersamaan. Tetapi kombinasi kedua obat ini tidak mencegah maupun memperbaiki kerusakan sendi karena pengendapan kristal dan memiliki resiko bagi penderita yang memiliki penyakit ginjal atau hati.