BELAJAR BERSAMA

swine influenza

2009-04-26T00:33:00.000-07:00

Swine Influenza (swine flu) is a respiratory disease of pigs caused by type A influenza that regularly cause outbreaks of influenza among pigs. Swine flu viruses do not normally infect humans, however, human infections with swine flu do occur, and cases of human-to-human spread of swine flu viruses has been documented.
Swine influenza virus (referred to as Swine influenza viruses or SIV) refers to influenza cases that are caused by Orthomyxoviruses endemic to populations of pigs. SIV strains isolated to date have been classified either as Influenzavirus C or one of the various subtypes of the genus Influenzavirus A.
Swine flu infects people every year and is found typically in people who have been in contact with pigs, although there have been cases of person-to-person transmission. Symptoms include: fever, disorientation, stiffness of the joints, vomiting, and loss of conciousness ending in death. Influenza A virus subtypes H1N1, H1N2, H3N1 and H3N2 are all known to cause SIV infections. and H2N3.

In swine, three influenza A virus subtypes (H1N1, H3N2, and H1N2) are circulating throughout the world. In the United States, the H1N1 subtype was exclusively prevalent among swine populations before 1998; however, since late August 1998, H3N2 subtypes have been isolated from pigs. Most H3N2 virus isolates are triple reassortants, meaning that it contains genes from human (HA, NA, and PB1), swine (NS, NP, and M), and avian (PB2 and PA) lineages.
In March and April 2009, more than 1,000 cases of swine flu in humans were detected in Mexico, and more than 80 deaths are suspected to have a connection with the virus. As of April 25, 2009 19:30 EDT there are 11 laboratory confirmed cases in the southwestern United States, New York City metropolitan area, and in Kansas. Following a series of reports of isolated cases of swine flu, the first announcement of the outbreak in Mexico was documented on April 23, 2009. Some of the cases have been confirmed by the World Health Organization to be due to a new genetic strain of H1N1. The new strain has been confirmed in 16 of the deaths and 44 others are being tested as of April 24, 2009. The Mexican fatalities are said to be mainly young adults, a hallmark of pandemic flu.

The new strain appears to be a recombinant between two older strains. Preliminary genetic characterization found that the hemagglutinin (HA) gene was similar to that of swine flu viruses present in U.S. pigs since 1999, but the neuraminidase (NA) and matrix protein (M) genes resembled versions present in European swine flu isolates. Viruses with this genetic makeup had not previously been found to be circulating in humans or pigs, but there is no formal national surveillance system to determine what viruses are circulating in pigs in the U.S.
The symptoms of swine flu in people are expected to be similar to the symptoms of regular human seasonal influenza and include fever, lethargy, lack of appetite and coughing. Some people with swine flu also have reported runny nose, sore throat, nausea, vomiting and diarrhea.
Influenza viruses can be directly transmitted from pigs to people and from people to pigs. Human infection with flu viruses from pigs are most likely to occur when people are in close proximity to infected pigs, such as in pig barns and livestock exhibits housing pigs at fairs. Human-to-human transmission of swine flu can also occur. This is thought to occur in the same way as seasonal flu occurs in people, which is mainly person-to-person transmission through coughing or sneezing of people infected with the influenza virus. People may become infected by touching something with flu viruses on it and then touching their mouth or nose.
There are four different antiviral drugs that are licensed for use in the US for the treatment of influenza: amantadine, rimantadine, oseltamivir and zanamivir. While most swine influenza viruses have been susceptible to all four drugs, the most recent swine influenza viruses isolated from humans are resistant to amantadine and rimantadine. At this time, CDC recommends the use of oseltamivir or zanamivir for the treatment and/or prevention of infection with swine influenza viruses.

flu singapura

2009-04-25T23:43:00.000-07:00

flu singapura sebenarnya adalah penyakit yang di dunia kedokteran dikenal sebagai hand, foot, and mouth disease (HMFD) atau penyakit kaki, tangan dan mulut (KTM).
penyakit KTM ini adalah penyakit infeksi yang disebabkan oleh virus RNA yang masuk dalam famili Picornaviridae,genus Enterovirus.Penyebab KTM yang paling sering pada pasien rawat jalan adalah Coxsackie A16, sedangkan yang sering memerlukan perawatan karena keadaannya lebih berat atau ada komplikasi sampai meninggal adalah Enterovirus 71.
penyakit ini sangat menular dan sering terjadi pada musim panas. penyakit ini biasa menyerang anak anak. orang dewasa umumnya kebal terhadap enterovirus.
penularan penyakit ini mmelalui kontak langsung dari orang ke orang yaitu melalui droplet,pilek,air liur,tinja,cairan dari vesikel atau ekskreta.penularan kontak tidak langsung melalui barang,handuk,baju,peralatan makan,mainan yang terkontaminasi oleh sekresi itu.pada penyakit ini tidak ada vektor tetapi ada pembawa/carier seperti lalat dan kecoa. penyakit ini mempunyai imunitas spesifik,namun anak dapat terkena penyakit ini kembali oleh vrus strain enterovirus lainnya.
gambaran klinik penyakit ini mula mula demam tidak tinggi 2-3 hari,diikuti sakit leher (pharingitis),tidak ada nafsu makan,pilek,gejala seperti flu. timbul vesikel yang kemudian pecah menjadi ulkus di mulut seperti sariawan teras nyeri hingga sukar menelan. bersamaan dengan itu timbul rash/ruam atau vesikel,papulovesikel yang tidak gatal di telapak tangan dan kaki. kadang kadang rash/ruam ada di bokong. penyakit ini membaik sendiri dalam 7-10 hari.
pada bayi/ anak dengan gejala berat atau dengan komplikasi harus dirawat di rumah sakit.
gejala berat antara lain adalah:
- hiperpireksia
- demam tidak turun turun
- tachicardia
- tachipneu
- malas makan,muntah atau diare dengan dehidrasi
- lethargia
- nyeri pada leher, lengan dan kaki
- kejang kejang
komplikasi penyakit ini adalah :
- meningitis
- enchepalitis
- myocarditis
- paralisis akut flaksid

TATALAKSANA :
o Istirahat yang cukup
o Pengobatan spesifik tidak ada.
o Dapat diberikan :
Immunoglobulin IV (IGIV), pada pasien imunokompromis atau neonatus
Extracorporeal membrane oxygenation.
o Pengobatan simptomatik :
-Antiseptik didaerah mulut
-Analgesik misal parasetamol
-Cairan cukup untuk dehidrasi yang disebabkan sulit minum dan karena demam
-Pengobatan suportif lainnya ( gizi dll )
Penyakit ini adalah self limiting diseases yang sembuh dalam 7-10 hari, pasien perlu istirahat karena daya tahan tubuh menurun. Pasien yang dirawat adalah yang dengan gejala berat dan komplikasi tersebut diatas.

PENCEGAHAN DAN PENGENDALIAN PENYAKIT:
Penyakit ini sering terjadi pada masyarakat dengan sanitasi yang kurang baik. Pencegahan penyakit adalah dengan menghilangkan Overcrowding, menjaga kebersihan (Higiene dan Sanitasi) lingkungan dan perorangan misal cuci tangan, desinfeksi peralatan makanan, mainan, handuk yang memungkinkan terkontaminasi.
Bila perlu anak tidak bersekolah selama satu minggu setelah timbul rash sampai panas hilang. Pasien sebenarnya tak perlu diasingkan karena ekskresi virus tetap berlangsung beberapa minggu setelah gejala hilang, yang penting menjaga kebersihan perorangan.
Di Rumah sakit Universal Precaution harus dilaksanakan.
Penyakit ini belum dapat dicegah dengan vaksin (Imunisasi)

Bronchitis

2009-03-14T02:28:00.000-07:00

Bronchitis is an inflammation of the air passages within the lungs. It occurs when the trachea (windpipe) and the large and small bronchi (airways) within the lungs become inflamed because of infection or other causes. When these tubes get infected, they swell and mucus (thick fluid) forms inside them. This makes it hard for you to breathe.

Symptoms include:
* Coughing up extra mucus, sometimes with blood
* Inflamation of the bronchus (lower trachea)
* Hardening (oedema) of the smooth muscle
* Blockage of the alvola
* Wheezing (bubbling - refered to as "bubble wrap effect" when heard with stethescope)
* Difficulty breathing (due to above symptoms)
* Blocked/Runny nose

Bronchitis can be acute or chronic. An acute medical condition comes on quickly and can cause severe symptoms, but it lasts only a short time (no longer than a few weeks). Acute bronchitis is most often caused by one of a number of viruses that can infect the respiratory tract and attack the bronchial tubes. Infection by certain bacteria can also cause acute bronchitis. Most people have acute bronchitis at some point in their lives.

Chronic bronchitis, on the other hand, can be mild to severe and is longer lasting — from several months to years. With chronic bronchitis, the bronchial tubes continue to be inflamed (red and swollen), irritated, and produce excessive mucus over time. The most common cause of chronic bronchitis is smoking.

People who have chronic bronchitis are more susceptible to bacterial infections of the airway and lungs, like pneumonia. (In some people with chronic bronchitis, the airway becomes permanently infected with bacteria.) Pneumonia is more common among smokers and people who are exposed to secondhand smoke.

Bronchitis is commonly treated with an antibiotic called Amoxicillin or with inhalers as with asthma. A rescue puffer, Ventolin, Salbutomal or Novo-Salmol, is commonly used for a respiratory emergency (dyspnea). Other inhalers can be prescribed for daily therapy use. When left untreated, or the infection spreads to the lower airways, it can often lead to Bronchiolitis which is more difficult to treat.

Chronic bronchitis is one sub-category of COPD (chronic obstructive pulmonary disease or disorder). Emphysema is another sub-category of COPD. With COPD, each interferes with the absorption of oxygen into the blood stream. COPD patients can degrade to the point where their breathing system does not recognize high levels of carbon dioxide buildup. Their breathing mechanism will respond to low levels of oxygen instead. So applying oxygen for treatment of a COPD patient can potentially shut down the respiratory drive. However, COPD is a secondary issue. The oxygen is required for treatment of the main injury or illness. The main point is to monitor and ensure that if the respiratory drive shuts down, rescue breathing or CPR can be immediately administered (if no signs of circulation). It is estimated that one in twenty smokers suffer from COPD (making it the main cause of the disease) most of which are middle aged men, smoking 20-40 cigarettes per day for a prolonged period of 20 years or more.

What's the best way to avoid getting bronchitis? Washing your hands often helps to prevent the spread of many of the germs that cause the condition — especially during cold and flu season.
If you don't smoke, don't ever start smoking — and if you do smoke, try to quit or cut down. Try to avoid being around smokers because even secondhand smoke can make you more susceptible to viral infections and increase congestion in your airway. Also, be sure to get plenty of rest and eat right so that your body can fight off any illnesses that you come in contact with.

common cold

2009-03-14T00:57:00.000-07:00

common cold is a highly contagious,viral infectious disease of the upper respiratory systems,primaly caused by picornaviruses(including rhinoviruses) or coronaviruses.
after initial infection,the viral replication cycle begins within 8 to 12 hours. symptoms can occur shortly thereafter,and usually begin within 2 to 5 days after infectioun,although occasionally in as little as 10 hours after infection.

the first indication of a cold is often a sore or scratchy throat. other common symptoms are a runny nose,congestion,sneezing,and cough. these are sometimes accompanied by muscle aches,fatigue,malaise,headache,weakness or loss of appetite. the symptoms usually resolve spontaneously in 7 to 10 days but some can last for up three weeks. symptoms may be more severe in infants,young children and tobacco users/smokers, and may include fiver and hives.

The common cold usually resolves spontaneously in 7 to 10 days but some symptoms can last for up to three weeks. There are no medications or herbal remedies proven to shorten the duration of illness. Treatment often is given via symptomatic supportive options, maximizing the comfort of the patient, and limiting complications and harmful sequelae.
The common cold is self-limiting, and the host's immune system effectively deals with the infection. Within a few days, the body's humoral immune response begins producing specific antibodies that can prevent the virus from infecting cells. Additionally, as part of the cell-mediated immune response, leukocytes destroy the virus through phagocytosis and destroy infected cells to prevent further viral replication. In healthy, immunocompetent individuals, the common cold resolves in seven days on average.

The National Institute of Allergy and Infectious Diseases suggests getting plenty of rest, drinking fluids to maintain hydration, gargling with warm salt water, using cough drops, throat sprays, or over-the-counter pain or cold medicines. Saline nasal drops may help alleviate congestion.
Treatment that may help alleviate symptoms include: analgesics, decongestants, and cough suppressants,[citation needed] first-generation anti-histamines such as brompheniramine, chlorpheniramine, diphenhydramine and clemastine (which reduce mucus gland secretion and thus combat blocked/runny noses but also may make the user drowsy). Second-generation anti-histamines do not have a useful effect on colds.

The best way to avoid a cold is to avoid close contact with existing sufferers; to wash hands thoroughly and regularly; and to avoid touching the eyes, nose, mouth, and face. Anti-bacterial soaps have no effect on the cold virus; it is the mechanical action of hand washing with the soap that removes the virus particles.
In 2002, the Centers for Disease Control and Prevention recommended alcohol-based hand gels as an effective method for reducing infectious viruses on the hands of health care workers. As with hand washing with soap and water, alcohol gels provide no residual protection from re-infection.
The common cold is caused by a large variety of viruses, which mutate quite frequently during reproduction, resulting in constantly changing virus strains. Thus, successful immunization is highly improbable.

osteoarthritis

2009-03-13T00:13:00.000-07:00

Osteoarthritis, sometimes called degenerative joint disease or osteoarthrosis, is the most common form of arthritis. Osteoarthritis occurs when cartilage in your joints wears down over time.
Osteoarthritis can affect any joint in your body, though it most commonly affects joints in your hands, hips, knees and spine. Osteoarthritis typically affects just one joint, though in some cases, such as with finger arthritis, several joints can be affected.
Osteoarthritis gradually worsens with time, and no cure exists. But osteoarthritis treatments can relieve pain and help you remain active. Taking steps to actively manage your osteoarthritis may help you gain control over your osteoarthritis pain.

Osteoarthritis usually develops in people who are over 50 years of age, and it is more common in women than in men. It is commonly thought that osteoarthritis is an inevitable part of getting older, but this is not true.
Younger people can also be affected by osteoarthritis, often as a result of an injury or another joint condition.
Osteoarthritis is often thought of as a critical and disabling condition, but this is not usually the case. The symptoms vary greatly from person to person, and between different affected joints.
There can also be variation between the amount of damage to the joints and the severity of the symptoms. For example, a joint may be severely damaged without causing symptoms, or symptoms may be severe without affecting the movement of a joint.
There is no cure for osteoarthritis, but the symptoms can be eased by using a number of different treatments. Mild symptoms can often be managed through exercise or by wearing suitable footwear. However, in more advanced cases of osteoarthritis other treatments may be necessary. Treatments include analgesics (painkillers), physiotherapy or surgery.

symptoms
The main symptoms of osteoarthritis are:
* pain,
* stiffness (which is worst when you wake up in the morning but improves within about 30 minutes when you start to move), and
* difficulty moving your affected joints.
Other symptoms of osteoarthritis may include:
* joint tenderness,
* increased pain and stiffness when you have not moved your joints for a while,
* joints appearing slightly larger, or more 'knobbly' than usual,
* a grating or crackling sound or sensation in your joints,
* limited range of movement in your joints,
* weakness and muscle wasting (loss of muscle bulk), and
* warm joints.

Symptoms of osteoarthritis in the knees
If you have osteoarthritis in your knees, it is likely that both of your knees will be affected, unless it has occurred as the result of an injury or another condition.
Your knees may be most painful when you walk, particularly when walking uphill or going up stairs. Sometimes your knees may 'give way' beneath you or lock into position so that you cannot straighten your legs. You may also hear a soft, grating sound when you move the affected joint.

Symptoms of osteoarthritis in the hips
Osteoarthritis in your hips often causes difficulty moving your hip joints. You may find it difficult to put your shoes and socks on or to get in and out of a car.
If you have osteoarthritis in your hips, you may have pain in your hips. However, it is quite common to have pain in your knee and not in your hip. Rarely, you may have pain in other areas such as the thighs, buttocks, knees and ankles. In most cases, pain will be at its worst when you walk, although it can also affect you when you are resting.

Symptoms of osteoarthritis in the hands
There are three main areas of your hand that are often affected by osteoarthritis - the base of your thumb, the joints closest to your fingertips, and the middle joints of your fingers.
Your fingers may become stiff, painful and swollen and you may develop bumps on your finger joints. However, over time the pain in your fingers may decrease and eventually disappear altogether, although the bumps and swelling may remain.
You may find that your fingers bend sideways slightly at your affected joints, or that you develop painful cysts (fluid-filled lumps) on the backs of your fingers.
In some cases you may also develop a bump at the base of your thumb where it joins your wrist. This can be painful and you may find it difficult to perform some manual tasks, such as writing, opening jars or turning keys.

treatment

conservative care
conservative measures such as weight control,appropiate rest and exercise, and the use of mechanical support devices are usually beneficial.regular exercise if possible, in the form of walking,swimming,or other low impact activities are encouraged.applying local heat before, and cold packs after exercise can help relieve pain and inflammation.

dietary
supplements which may be useful for treating OA include: glucosamine,chondroitin,omega-3 fatty acid,folic acid,cobalamine.

specific medication
-paracetamol treat the pain from OA
-nsaid(non steroidal anti inflammatory drugs) may reduce both the pain and inflammation.most prominent drugs in thhe class include diclofenac,ibuprofen,naproxen,ketoprofen.
-COX-2 selective inhibitors such as selecoxib,rofecoxib,valdecoxib.
-corticosteroid
-narcotics for moderate to severe pain, narcotic pain relievers such as tramadol,and eventually opioids may be necessary
if the mangement above in inefective,joint replacement surgery may be required

Chronic renal failure

2009-02-21T23:13:00.000-08:00

Chronic renal failure (CRF) is the progressive loss of kidney function. The kidneys attempt to compensate for renal damage by hyperfiltration (excessive straining of the blood) within the remaining functional nephrons (filtering units that consist of a glomerulus and corresponding tubule). Over time, hyperfiltration causes further loss of function.
Chronic loss of function causes generalized wasting (shrinking in size) and progressive scarring within all parts of the kidneys. In time, overall scarring obscures the site of the initial damage. Yet, it is not until over 70% of the normal combined function of both kidneys is lost that most patients begin to experience symptoms of kidney failure.

Types
Chronic renal failure (CRF) can be classified by the site (location) of primary damage:
* Pre-renal CRF
* Post-renal CRF (obstructive uropathy)
* Renal CRF

Causes
The cause for CRF sometimes can be determined by a detailed medical history, a comprehensive physical examination, and laboratory studies. More often than not, determining the cause of CRF is difficult if not impossible. Even a kidney biopsy may be inconclusive, because all forms of kidney failure eventually progress to diffuse scarring and look the same on kidney biopsy. The most common causes for CRF are diabetes and high blood pressure (hypertension.)
Kidney disorders, including chronic renal failure, are common in patients who have multiple myeloma (cancer that begins in a type of white blood cell called plasma cells). Several different factors are related to renal disease associated with multiple myeloma. Myeloma cells produce large numbers of proteins in the urine (called proteinuria). These proteins often form deposits in the kidneys (condition called amyloidosis) and cause kidney failure. In addition, multiple myeloma increases the risk for hypercalcemia (high levels of calcium in the blood) and anemia (low levels of red blood cells) and results in high blood levels of uric acid, which also increase the risk for chronic renal failure.

Pre-Renal CRF
Some medical conditions cause continuous hypoperfusion (low blood flow) of the kidneys, leading to kidney atrophy (shrinking), loss of nephron function, and chronic renal failure (CRF). These conditions include poor cardiac function, chronic liver failure, and atherosclerosis ("hardening") of the renal arteries. Each of these conditions can induce ischemic nephropathy.

Post-Renal CRF
Interference with the normal flow of urine can produce backpressure within the kidneys, can damage nephrons, and lead to obstructive uropathy, a disease of the urinary tract. Abnormalities that may hamper urine flow and cause post-renal CRF include the following:
* Bladder outlet obstruction due to an enlarged prostate gland or bladder stone
* Neurogenic bladder, an overdistended bladder caused by impaired communicator nerve fibers from the bladder to the spinal cord
* Kidney stones in both ureters, the tubes that pass urine from each kidney to the bladder
* Obstruction of the tubules,the end channels of the renal nephrons
* Retroperitoneal fibrosis, the formation of fiberlike tissue behind the peritoneum, the membrane that lines the abdominal cavity
* Vesicoureteral reflux (VUR), the backward flow of urine from the bladder into a ureter

Renal CRF
Chronic renal failure caused by changes within the kidneys, is called renal CRF, and is broadly categorized as follows:
* Diabetic nephropathy, kidney disease associated with diabetes; the most common cause of CRF
* Hypertension nephrosclerosis, a condition that occurs with increased frequency in African Americans; the second leading cause of CRF
* Chronic glomerular nephritis, a condition caused by diseases that affect the glomeruli and bring about progressive dysfunction
* Chronic interstitial nephritis, a condition caused by disorders that ultimately lead to progressive scarring of the interstitium
* Renal vascular CRF, large vessel abnormalities such as renal artery stenosis (narrowing of the large arteries that supply the kidneys)
* Vasculitis, inflammation of the small blood vessels
* Cystic kidney disease, kidney disease distinguished by multiple cysts (lined cavities or sacs)
* Hereditary diseases of the kidney, such as Alport's syndrome (hereditary nephritis)

Signs and Symptoms
Chronic renal failure (CRF) usually produces symptoms when renal function — which is measured as the glomerular filtration rate (GFR) — falls below 30 milliliters per minute (< 30 mL/min).This is approximately 30% of the normal value.
When the glomerular filtration rate (GFR) slows to below 30 mL/min, signs of uremia (high blood level of protein by-products, such as urea) may become noticeable. When the GFR falls below 15 mL/min most people become increasingly symptomatic.
Uremic symptoms can affect every organ system, most noticeably the following:
* Neurological system–cognitive impairment, personality change, asterixis (motor disturbance that affects groups of muscles), seizures (rare)
* Gastrointestinal system–nausea, vomiting, food distaste (often described as bland, metallic, "like cardboard")
* Blood-forming system–anemia due to erythropoetin deficiency, easy bruising and bleeding due to abnormal platelets
* Pulmonary system–fluid in the lungs, with breathing difficulties
* Cardiovascular system –chest pain due to inflammation of the sac surrounding the heart (pericarditis) and pericardial effusion (fluid accumulation around the heart)
* Skin –generalized itching

Diagnosis
Chronic renal failure (CRF) is diagnosed by the observation of a combination of symptoms and elevated blood urea nitrogen (BUN) and creatinine (Cr) levels. The following abnormalities found in the blood may signal CRF:
* Anemia (low red blood cell count)
* High level of parathyroid hormone
* Hypocalcemia (low blood level of calcium)
* Hyperphosphatemia (high blood level of phosphate)
* Hyperkalemia (high blood level of potassium)
* Hyponatremia (low blood level of sodium)
* Low blood level of bicarbonate
* Low plasma pH (blood acidity)
Whether renal failure is acute or chronic usually can be distinguished by comparing prior test results (e.g., from the past several months or years). It is difficult to make the distinction without previous test results.
Ultrasound may show that the kidneys are small in size and echogenic (a sign of renal scarring), signs that supports a diagnosis of CRF. For unclear reasons patients with diabetic nephropathy often have preservation of kidney size despite CRF. They do however, typically have increased echogenicity.

Treatment
Once CRF has been diagnosed, the physician attempts to determine the cause and, if possible, plan a specific treatment. Nonspecific treatments are implemented to delay or possibly arrest the progressive loss of kidney function.
Control hypertension (high blood pressure)—Target systolic blood pressure (BP) is 120 to 135 mm Hg; target diastolic BP is 70 to 80 mm Hg. Antihypertensive medication from the ACE class is preferable because of protective effects on the kidneys.
Restrict dietary protein—Dietary protein is broken down into amino acids and absorbed from the stomach into the blood. The amino acids are taken from the bloodstream and used to build muscle and perform other essential functions. Excess amino acids are further broken down into carbohydrates and nitrogen-containing waste that is eliminated by the kidneys. Amino acid disposal further burdens the kidneys, and is believed to speed the progression of CRF. This process is like forcing a damaged machine to work harder, causing it to break down sooner than expected.
Affected patients must be cautious not to overdo protein restriction, because it can lead to malnutrition and muscle wasting. Moderate protein restriction for a CRF patient is about 0.6 to 0.8 gm/kg/day, which is effectively achieved by following the advice of a dietician.
Manage pre-end-stage renal disease (pre-ESRD)—Treatment for pre-ESRD should begin once the glomerular filtration rate (GFR) falls below 30 milliliters per minute (< 30 mL/min). Pre-ESRD management includes the identification and treatment of anemia (low red blood cell count). When the GFR drops below 30 mL/min, anemia often develops because the kidneys produce an inadequate amount of erythropoetin (EPO). This hormone is made by the kidneys and travels to the bone marrow, where it stimulates red blood cell production. Anemic patients are candidates for EPO (Procrit®) injections to maintain their hematocrit (volume percent of red blood cells in whole blood) between 30% and 36%.
Identify and Treat Secondary Hyperparathyroidism—With the loss of kidney function, phosphate accumulates in the blood. Excess phosphate in the blood reduces levels of blood calcium, and low blood calcium levels trigger the parathyroid gland (located in the neck) to release more parathyroid hormone (PTH). PTH then dissolves bone tissue to release stored calcium and raise the level of calcium in the blood. This chronic cycle of events is called secondary hyperthyroidism.
The net result of this condition is the development of metabolic bone disease (renal osteodystrophy). These patients are at risk for bone fractures, bone and muscle pain, which can sometimes be accompanied by severe itching, and cardiovascular complications. Severe itching is thought to be in part due to the elevated circulating PTH level itself.
Patients with secondary hyperthyroidism should limit their intake of foods that are high in phosphate (e.g., dairy products, colas). Many patients must take medication with meals that binds the phosphate (phosphate-binders) and prevents it from being absorbed into the blood and allows it to be excreted in the stool (feces). In general, calcium based salts (e.g., TUMS, Oscal)have been the phosphate-binders prescribed. A new organic based phophate-binder called renagel has recently become available and, although it is more expensive, it has many advantages over the calcium based phosphate-binders.
Most patients also require a potent vitamin D supplement (e.g., calcitrol, hexitrol), which helps to suppress excess PTH production. The final metabolic step in the synthesis of vitamin D occurs normally in the kidney and there is often a deficiency of this vitamin in these patients.
Cinacalcet hydrochloride (e.g., Sensipar™) may be used alone or in combination with Vitamin D supplements or phosphate-binders to treat patients with secondary hyperparathyroidism who are on dialysis. Sensipar tablets should be taken with food and the dosage varies, depending on calcium and phosphate levels in the blood. Side effects include nausea, vomiting, and diarrhea.
Preparation for renal replacement therapy (RRT)
Early preparation is important. The health care team educates the patient about the different procedures involved in RRT, which include the following:
* Hemodialysis—removal of toxic elements from the blood, which is filtered through a membrane while circulated outside of the body
* Peritoneal dialysis—filtration through the lining membrane of the abdominal cavity; fluid is instilled into the peritoneal space, then drained
* kidney transplantation
It is important to place an arteriovenous fistula (AVF)—a passage between an artery and a vein that provides a suitable blood vessel for repeated dialysis—at least 3 months prior to beginning hemodialysis, because an AVF requires 3 months to mature before it can be used.
The health care team can address the patient's fears and anxieties about treatment and can clarify the financial, emotional, and social concerns of RRT.
Prognosis
CRF is often insidious in its onset and progression. The rate of progression is variable but usually renal function steadily declines resulting in end-stage renal disease (ESRD).

first experience

2007-11-15T17:59:00.000-08:00

lebih dari setengah tahun ini aku lebih memilih memberikan seluruh waktu n perhatianku buat melihat pertumbuhan dan perkembangan si kecil,buah hatiku..... n sekarang saat aku ngerasa udah waktunya aku harus mulai nyoba cari pengalaman buat mengasah ilmu yang pernah aku pelajari,aku cobalah mulai ngelamar kerja jadi dokter jaga di sebuah rumah sakit di deket rumah,alhamdulillah diterima,jadilah aku mulai kerja.

seminggu aku kerja 3 hari,2 hari jaga pagi dan seharinya lagi jaga malam.... juga kadang2 ngegantiin dokter2 jaga lain yang berhalangan masuk,buat aku sih kerja seminggu 3 hari juga udah cukup,lumayan buat tambah2 pengalaman,lagipula anak aku masih 7 bulan,rasanya kasian juga kalo sering2 ditinggal,masalahnya dirumah sakit tempat aku kerja, sehari cuma dibagi 2 shift dokter jaga,jadi ya.... itung aja sehari berapa lama jam kerjanya.

pertama kali aku masuk kerja aku dapet giliran jaga bangsal,kagok juga sih awalnya.... tapi yah... sok pede aja... pokoknya aku minta dibantu sama perawat n dokter2 disana.
awal2 sih kasusnya gak gitu aneh2,masih seputar GE,febris typhoid,KP,brpn,masih aman lah....

trus setelah beberapa kali jaga mulailah bermunculan kasus kasus yang butuh perhatian besar,mulai dari tetanus,meningitis,cks,ileus,leukemia,thalasemia,stroke,intoksikasi obat hama n bensin,SN,GGK dll.... jadilah aku mulai belajar n belajar lagi,buka buka buku lagi,tanya sana sini lagi... oya aku kadang juga suka main2 ke vk, liat2 kasus kebidanan,untung dokter obgin nya baik,jadi aku boleh ikutan nongkrong di vk belajar kasus2 kebidanan,maklum lah waktu masih koas kebidanan,ilmu n skill ku minim banget,partus pandang,manual plasenta pandang,vakum pandang,segalanya serba dipandang lah pokoknya....hai hai para dokter yang baru lulus n baru mulai kerja... mari kita saling berbagi pengalaman.... oke...

DIARE PADA ANAK

2007-09-25T22:54:00.000-07:00

diare adalah pola defekasi yang abnormal,dimana frekwensinya meningkat,lebih dari 4 kali dalam sehari,dengan konsistensi yang lebih cair dari pada biasanya. Tetapi perlu diingat bahwa pada bayi yang mendapatkan asi ekslusif frekwensi defekasi 5-6 kali sehari masih dianggap normal.
diare akut pada anak biasanya disebabkan karena infeksi,tetapi selain itu juga bisa disebabkan karena malabsorpsi dan enteropati. Sejauh ini komplikasi dari diare yang paling sering terjadi adalah dehidrasi.
patofisiologi dari diare bisa bermacam macam,virus dapat secara langsung menyababkan kerusakan di dinding usus sehingga meningkatkan sekresinya,rotavirus memproduksi endotoksin yang dapat memicu sekresi dari usus halus sehingga mengakibatkan tinja yang cair,bakteri dapat menyebabkan terjadinya ulserasi dan abses di dinding usus.
gejala klinis
selain diare juga bisa terdapat gejala gejala berikut:
1. dehidrasi
Dehidrasi adalah penyebab terbanyak kematian pada diare,setiap pasien diare harus dinilai derajat dehidrasinya. letargi,penurunan kesadaran,ubun ubun yang cekung,mukosa membran yang kering,tidak ada air mata,turgor kulit menurun,capillary refill yang terlambat, semua itu adalah beberapa tanda penting dehidrasi
2.malnutrisi
3. abdominal pain
4.peristaltik yang meningkat
5.perianal erythemamedical care
karena kebanyakan diare adalah self limiting disease,maka terapi yang utama adalah bersifat suportif,yaitu memelihara cairan dan menterapi dehidrasi. terapi rehidrasi oral adalah terapi pertama pada diare anak,terapi rehidrasi intravena dikerjakan bila terapi rehidrasi oral dirasa tidak berhasil
1.terapi rehidrasi oral
2.pemberian makan/asi lebih sering dari biasanya
3.obat spasmolitik tidak diindikasikan untuk diare karena infeksi
4.anti mikroba diindikasikan untuk nonviral diare
Aeromonas species:Use cefixime and most third- and fourth-generation cephalosporins.
Campylobacter species:Erythromycin shortens illness duration and shedding.
C difficile:Discontinue potential causative antibiotics.
If antibiotics cannot be stopped or this does not result in resolution, use oral metronidazole or vancomycin. Vancomycin is reserved for the child who is seriously ill.
C perfringens:Do not treat with antibiotics.
Cryptosporidium parvum:Paromomycin; however, effectiveness is not proven. Nitazoxanide, a newer anthelmintic, is effective against C parvum.
Entamoeba histolytica:Metronidazole followed by iodoquinol or paromomycin Asymptomatic carriers in nonendemic areas: Iodoquinol or paromomycin.
E coli:Trimethoprim-sulfamethoxazole (TMP-SMX) if moderate or severe; antibiotic treatment may increase likelihood of HUS. Parenteral second-generation or third-generation cephalosporin for systemic complications
G lambli:Metronidazole or nitazoxanide can be used.
Plesiomonas species:Use TMP-SMX or any cephalosporin.
Salmonella species:Treatment prolongs carrier state, is associated with relapse, and is not indicated for nontyphoid-uncomplicated diarrhea. Treat infants younger than 3 months and high-risk patients (eg, immunocompromised, sickle cell disease). TMP-SMX is first-line medication; however, resistance occurs. Use ceftriaxone and cefotaxime for invasive disease.
Shigella species:Treatment shortens illness duration and shedding but does not prevent complications. TMP-SMX is first-line medication; however, resistance occurs. Cefixime, ceftriaxone, and cefotaxime are recommended for invasive disease.
V cholerae:Treat infected individuals and contacts. Doxycycline is the first-line antibiotic, and erythromycin is second-line antibiotic.
Yersinia species:TMP-SMX, cefixime, ceftriaxone, and cefotaxime are used. Treatment does not shorten disease duration; reserve for complicated cases.

macam obat

1.cefixime:potensial long akting sefalosporin
dosis dewasa: 400mg po 4xsehari 7-10 hari
dosis anak:8mg/kgbb po 4xsehari 7-10 hari
umumnya aman untuk wanita hamil
ki:alergi penisilin,ggg fx ginjal
2.seftriakson:
sefalosporin generasi ketiga
dosis dewasa 1-2 g IV/IM dalam 24 jam
dosis anak 50mg/kgbb/hari IV/IM 2-4xsehari
ki:riwayat alergi,hiperbilirubin
umumnya aman untuk wanita hamil
3.cefotaxim:
sefalosporin generasi ketiga
dosis dewasa 1-2 g IV/IM dalam 24 jam
dosis anak 50mg/kgbb/hari IV/IM 2-4xsehari
ki:riwayat alergi penisilin
umumnya aman untuk wanita hamil
4. eritromisin:
makrolide bakteriostatik,berguna untuk kuman vibrio dan csmpylobscter
dosis dewasa 250-500mg po 4x sehari
dosis anak 50mg/kgbb/hari po/iv dibagi dalam 4x sehari
ki riw alergi,ggg hati
umumnya aman untuk wanita hamil
5.metronidazole:
aktif untuk spesies giardia,entamoeba
dosis dewasa 250-500 po 3xsehari 10 hari
dosis anak3050mg/kgbb/hari po
6.kotrimoksasol:
efektiv untuk E coli
dosis dewasa 160 mg po 2xsehari 7-10 hari
dosis anak 10 mg/kgbb/ hari po dibagi 2 dosis
7.tetrasiklin
dosis dewasa 25-500 mg po 4xsehari selama 6 hari
dosis anak >8 tahun 25-50mg/kgbb/hari
tidak aman untuk wanita hamil
8.vankomisin
efektiv untuk C difficile
dosis dewasa 500mg po 4xsehari
dosis anak 40-50 mg/kgbb/hari

asthma !!!!!!

2007-08-13T06:34:00.001-07:00

Asthma is a chronic disease of the respiratory system in which the airway occasionally constricts, becomes inflamed, and is lined with excessive amounts of mucus, often in response to one or more triggers( such as exposure to an environmental stimulant (or allergen), cold air, warm air, moist air, exercise or exertion, or emotional stress). Between episodes, most patients feel well but can have mild symptoms and they may remain short of breath after exercise for longer periods of time than the unaffected individual.
sign and symptoms:
1. shortness of breath (dyspnea) and either wheezing or stridor
2. some patients present primarily with coughing
3. sometimes produce clear sputum
4. wheezing, rapid breathing (tachypnea), prolonged expiration, a rapid heart rate (tachycardia), rhonchous lung sounds (audible through a stethoscope), and over-inflation of the chest.
5. accessory muscles of respiration (sternocleidomastoid and scalene muscles of the neck) may be used,shown as in-drawing of tissues between the ribs and above the sternum and clavicles
6. paradoxical pulse (a pulse that is weaker during inhalation and stronger during exhalation).
7. During very severe attacks, an asthma sufferer can turn blue from lack of oxygen, and can experience chest pain or even loss of consciousness

Treatment
1. The most effective treatment for asthma is identifying triggers,and limiting or eliminating exposure to them. Desensitization to allergens has been shown to be a treatment option for certain patients.
2. Relief medication:
a.Short-acting, selective beta2-adrenoceptor agonists, such as salbutamol
b.Older, less selective adrenergic agonists, such as inhaled epinephrine and ephedrine
c.Anticholinergic medications, such as ipratropium bromide may be used
d.Inhaled glucocorticoids are usually considered preventive medications
3. Prevention medication:
a.Inhaled glucocorticoids (ciclesonide, beclomethasone, budesonide, flunisolide, fluticasone, mometasone, and triamcinolone).
b.Leukotriene modifiers (montelukast, zafirlukast, pranlukast, and zileuton).
c.Mast cell stabilizers (cromoglicate (cromolyn), and nedocromil).
d.Antimuscarinics/anticholinergics (ipratropium, oxitropium, and tiotropium), which have a mixed reliever and preventer effect. (These are rarely used in preventive treatment of asthma, except in patients who do not tolerate beta-2-agonists.)
e.Methylxanthines (theophylline and aminophylline)
f.Antihistamines
g.Omalizumab, an IgE blocker,Methotrexate,
4. Long-acting β2-agonists
Long-acting bronchodilators (LABD) are similar in structure to short-acting selective beta2-adrenoceptor agonists, but have much longer sidechains resulting in a 12-hour effect, and are used to give a smoothed symptomatic relief (used morning and night). Currently available long-acting beta2-adrenoceptor agonists include salmeterol, formoterol, bambuterol, and sustained-release oral albuterol.

Emergency treatment
When an asthma attack is unresponsive to a patient's usual medication, other treatments are available to the physician or hospital:
a. oxygen to alleviate the hypoxia (but not the asthma per se) that results from extreme asthma attacks;
b. nebulized salbutamol or terbutaline (short-acting beta-2-agonists), often combined with ipratropium (an anticholinergic);
c. systemic steroids, oral or intravenous (prednisone, prednisolone, methylprednisolone, dexamethasone, or hydrocortisone). Some research has looked into an alternative inhaled route.[44]
d. other bronchodilators that are occasionally effective when the usual drugs fail:
o intravenous salbutamol
o nonspecific beta-agonists, injected or inhaled (epinephrine, isoetharine, isoproterenol, metaproterenol);
o anticholinergics, IV or nebulized, with systemic effects (glycopyrrolate, atropine, ipratropium);
o methylxanthines (theophylline, aminophylline);
o inhalation anesthetics that have a bronchodilatory effect (isoflurane, halothane, enflurane);
o the dissociative anaesthetic ketamine, often used in endotracheal tube induction
o magnesium sulfate, intravenous; and
e. intubation and mechanical ventilation, for patients in or approaching respiratory arrest.
f. Heliox, a mixture of helium and oxygen, may be used in a hospital setting. It has a more laminar flow than ambient air and moves more easily through constricted airways

ASPEK SEROLOGIK RADANG HATI VIRUS

2007-06-21T08:10:00.000-07:00

radang hati virus adalah radang hati yang disebabkan oleh karena hepatotropik virus,dimana organ hati merupakan sasaran yang utama.
kini telah dikenal minimal lebih dari tujuh virus penyebab radang hati,diantaranya:
1. virus hepatitis A
2. virus hepatitis B
3. virus hepatitis C
4. virus hepatitis D
5. virus hepatitis E
6. virus hepatitis F
7. virus hepatitis G
semua virus tersebut diatas dapat menyebabkan keadaan hepatitis akut dengan manifestasi klinik yang bervariasi,mulai dari tanpa gejala sampai gejala yang paling berat,bahkan sampai kematian.

1. Virus Hepatitis A
parameter diagnostik laboratorium untk hepatitis virus A adalah HAV antigen dan anti-HAV. antigen HAV sudah dapat dijumpai pada tinja pada fase inkubasi dan fase akut,al ini penting dalam proses penularan virus melalui fekal-oral. antigen HAVdalam tinja dapat dideteksi denan perantara IEM,RIA, atau ELISA. namun yang lebih praktis adalah deteksi antibodi HAV.anti HAV sudah timbul pada fase akut,jenis anti HAV yang pertama muncul adalah IgM anti HAv,baru kemudian disusul IgG anti HAV. IgM anti HAV dapat menetap 2-3 bulan,sedangkan IgG anti HAV dapat bertahan hingga bertahun tahun.

2. Virus Hepatitis B
perubahan serologik pada hepatitis virus B dimulai dengan timbulnya HBsAg/HBeAg/HBV DNA dalam darah/serum,sering mendahului peningkatan enzim transaminase,kemudian berturut turut disusul dengan timblnya IgM anti HBeAg dan anti HBs. perubahan serologik pada infeksi hepatitis B umumnya akan kembali dalam waktu kurang dari 6 bulan,dikatakan kronis bila perubahan serologis menetap hingga lebi dari 6 bulan. terjadinyakeganasan kanker hati primer,perlu diwaspadai bila kadar alfafetoprotein>300ng/ml,persangkaan diagnosis bila kadar AFP>500ng/ml lebih2 bila AFP>100ng/ml

3. Virus Hepatitis C ditandai dengan timbulnya HCV RNA pada fase dini,sebelum terjadinya peningkatan aktivitas serum transaminase yang karakteristik fluktuatif,kemudian disusul dengantimbulnya anti HCV yang lebih lambat.penjalaran hepatitis virus C akut 50% akanmenjadikronis dan 20% akan menjadi sirosis,waktu rata2 untuk timbulnya sirosis pada infeksi HCV sekitar 20 tahun.

4. Virus hepatitis Delta
virus hepatitis delta merupakan virus detetif,yang membutukan komponen HBV untuk replikasinya. pada akut delta ko-infeksi akandijimpai aktivitas seru enzimtransaminase yang bifasik,dan kadar HBsAg yan menurun,diagnosis adanya hepatitis virus delta dapat melalui deteksi HDAg pada jaringan hati/darah atau serum IgM anti HDV

5.Virus Hepatitis E
perubahan serologi pada infeksi HEV menyerupai hepatitis A,dan diagnosis adanya hepatitis E akut dapat dibuat melalui pemeriksaan HEV RNA dalam tinja dengan metode IEM maupun PCR atau melalui pemeriksaan IgM antiHEV serum

PERDARAHAN ANTEPARTUM

2007-06-18T04:39:00.000-07:00

I. Definisi
Definisi perdarahan antepartum menurut WHO adalah perdarahan pervagina setelah 29 minggu kehamilan atau lebih
II. Klasifikasi
Klasifikasi penyebab perdarahan antepartum antara lain yaitu :
1. Plasenta previa
2. Solusio plasenta
3. Perdarahan antepartum yang tidak jelas sumbernya (idiopatik)
III. Perbedaan antara solutio plasenta dan plasenta previa
a).Ciri-ciri plasenta previa :
1. Perdarahan tanpa nyeri
2. Perdarahan berulang
3. Warna perdarahan merah segar
4. Adanya anemia dan renjatan yang sesuai dengan keluarnya darah
5. Timbulnya perlahan-lahan
6. Waktu terjadinya saat hamil
7. His biasanya tidak ada
8. Rasa tidak tegang (biasa) saat palpasi
9. Denyut jantung janin ada
10. Teraba jaringan plasenta pada periksa dalam vagina
11. Penurunan kepala tidak masuk pintu atas panggul
12. Presentasi mungkin abnormal.
b).Ciri-ciri solusio plasenta :
1. Perdarahan dengan nyeri
2. Perdarahan tidak berulang
3. Warna perdarahan merah coklat
4. Adanya anemia dan renjatan yang tidak sesuai dengan keluarnya darah
5. Timbulnya tiba-tiba
6. Waktu terjadinya saat hamil inpartu
7. His ada
8. Rasa tegang saat palpasi
9. Denyut jantung janin biasanya tidak ada
10. Teraba ketuban yang tegang pada periksa dalam vagina
11. Penurunan kepala dapat masuk pintu atas panggul
12. Tidak berhubungan dengan presentasi
IV. Pengelolaan
a). plasenta previa
Pengelolaan plasenta previa tergantung dari banyaknya perdarahan, umur kehamilan dan derajat plasenta previa.
ibu yang dicurigai plasenta previa harus dikirim ke rumah sakit yang memiliki fasilitas untuk transfusi darah dan operasi. Sebelum penderita syok, pasang infus NaCl/RL sebanyak 2 -3 kali jumlah darah yang hilang. Jangan melakukan pemeriksaan dalam atau tampon vagina, karena akan memperbanyak perdarahan dan menyebabkan infeksi
1. Konservatif bila :
a. Kehamilan kurang 37 minggu.
b. Perdarahan tidak ada atau tidak banyak (Hb masih dalam batas normal).
c. Tempat tinggal pasien dekat dgn rumah sakit (dapat menempuh perjalanan selama 15 mnt)
2. Penanganan aktif bila :
a. Perdarahan banyak tanpa memandang usia kehamilan.
b. Umur kehamilan 37 minggu atau lebih.
c. Anak mati
Perawatan konservatif berupa :
- Istirahat.
- Memberikan hematinik untuk mengatasi anemia dan tokolitik
- Memberikan antibiotik bila ada indikasi.
- Pemeriksaan USG, Hb, dan hematokrit.
Bila selama 3 hari tidak terjadi perdarahan setelah melakukan perawatan konservatif maka lakukan mobilisasi bertahap. Pasien dipulangkan bila tetap tidak ada perdarahan.
Penanganan aktif berupa :
- Persalinan per vaginam.
- Persalinan per abdominal.
Indikasi persalinan pervaginam
-plasenta previa marginalis
-plasenta previa letak rendah
-plasenta previa lateralis dengan pembukaan 4 cm/lebih.
Pada kasus tersebut bila tidak banyak perdarahan maka dapat dilakukan pemecahan kulit ketuban agar bagian bawah anak dapat masuk pintu atas panggul menekan plasenta yang berdarah. Bila his tidak adekuat dapat diberikan pitosin drip. Namun bila perdarahan tetap ada maka dilakukan seksio sesar
Indikasi melakukan seksio sesar :
- Plasenta previa totalis
- plasenta previa lateralis dimana perbukaan <4>
- Perdarahan banyak tanpa henti.
- Presentase abnormal.
- Panggul sempit.
- Keadaan serviks tidak menguntungkan (beelum matang).
- Gawat janin
b).solutio plasenta
Setiap pasien yang dicurigai solusio plasenta harus dirujuk ke spesialis karena memerlukan monitoring yang lengkap baik dalam kehamilan maupun persalinan
1.Bila umur kehamilan <37 solusio plasenta ringan,terapi konservatif
2.Bila umur kehamilan <37 solusio plasenta sedang dan berat/ringan yg memburuk,persalinan pervaginam bila persalinan diperkirakan <6 jam
3.Bila umur kehamilan >37 minggu/TBF 2500 g seksio sesar diindikasikan jika persalinan pervagina diperkirakan berlangsung lama baik pada solusio plasenta ringan, sedang maupun berat.
4.Pasien dengan solusio plasenta sedang/berat, tranfusi darah atau resusitasi cairan hendaknya dilakukan terlebih dahulu sebelum tindakan obstetri. Ketuban dapat segera dipecah tanpa memperdulikan apakah persalinan pervagina atau perabdominal untuk mengurangi regangan uterus