Thursday, March 25, 2010

Dah dapat gaji...hehehe

Asslalamualaikum....hahahah...wah..wah..ari nih boleh gelak besaq dah...pasai apa? pasai hari ni kerabat kakitangan kerajaan dah dapat gaji...yerlah....last gaji diterima 8/2/2010 ari tu....dekat nak masuk 2 bulan gaji kena ari nih leh makan besaq...ader kawan2 kita dah gi makan secret recipe...belanja sakan..takper lah apa2 pon selamat....cite2 pasal tak der duit hari tu....hari khamis minggu lepas kita cuti...pasal baby faris demam...dok jga dia kat umah...abih tu abang ngan angah tak mo gi umah toksu...dok lah ngan nih kalu demam...mak ai merengek dia memang teruk...asyik berdokong jer...

hari jumaat tuh...mak mertua kita tipon nak datang...aper lagi kita anak beranak kelam kabut kemas umah..maklomlah baby dah buat perangai...umah tak berkemas aper lagi umah cam tongkang pecah lah...sib baik hubby tolong sama....petang tu deme sampai umah next n3 plak kita cite apa aktiviti yangkita buat masa mak mertuaku datang ke umah jumpa lagi...

Wednesday, March 17, 2010


Pulmonary atresia is a very rare type of congenital heart defect in which the pulmonic valve is permanently closed or completely absent from the heart. This valve is located between the right ventricle and the pulmonary artery. It is responsible for opening and closing at precise moments to allow blood to flow from the heart through the pulmonary artery and to the lungs, where it is infused with oxygen. When the pulmonic valve completely malfunctions, oxygen-poor blood cannot reach the lungs and, therefore, cannot be oxygenated.

The symptoms of pulmonary atresia typically appear shortly after birth. The most obvious sign is a baby who appears cyanotic (known as blue baby), indicating the lack of sufficient oxygen in the blood. The degree of cyanosis will vary depending on the presence of other conditions, such as a patent ductus arteriosus - another heart defect that allows oxygen-poor and oxygen-rich blood to mix. Other symptoms may include breathing difficulties, lethargy and pale skin color.

During a physical examination of a patient with suspected pulmonary atresia, a cardiologist may detect a heart murmur through a stethoscope. To help diagnose the condition, a number of tests may be ordered including a chest x-ray, electrocardiogram (EKG) and cardiac magnetic resonance imaging (MRI). In addition, cardiac catheterization may be used to evaluate this and other heart defects that may exist in the patient.

Treatment for pulmonary atresia is determined by the age and overall health of the patient, as well as the severity of the defect and tolerance for treatment. Early treatment for pulmonary atresia may include a drug that prevents the patent ductus arteriosus from closing. Surgery is typically needed to treat pulmonary atresia. The type of corrective surgery that will be performed depends greatly on what other heart defects are present.

Without treatment, a patient’s chance of long-term survival is poor because the body cannot get enough oxygen-rich blood. Fortunately, the treatments available offer patients a greater chance of a healthy and active life.


About single ventricle

Single ventricle is a rare type of heart condition present at birth (congenital heart disease), in which the patient’s heart has only one large pumping chamber (ventricle). Normally, this pumping chamber is divided into two separate smaller chambers: The left ventricle and the right ventricle. The left ventricle would normally receive oxygen-rich blood from the left atrium, while the right ventricle would normally receive oxygen-poor blood from the right atrium. Thus, in a normal heart oxygen-rich and oxygen-poor blood never mix.

In a single ventricle, by contrast, oxygen-rich blood from the lungs and oxygen-poor blood from the body are allowed to freely mix before being pumped from the heart. As a result, some oxygen-rich blood needlessly travels back to the lungs, and some oxygen-poor blood uselessly travels to the rest of the oxygen-demanding body.

This condition causes abnormal blood flow, a lack of oxygen-rich blood flow to the body and increased pressure throughout the circulatory system. Because of the lack of oxygen, the baby is born with a bluish tint (cyanosis) to its skin, lips, fingernails and other areas of the body. This condition is referred to as blue baby. Untreated, single ventricle can result in heart failure or even death.

It is not fully understood what causes a single ventricle to develop, although scientists suspect that the defect may be the result of genetic alterations.

Signs and symptoms of single ventricle

One sign of single ventricle is cyanosis – a bluish tint to the child’s skin, lips, fingernails and other parts of the body (often called blue baby). Other possible signs of single ventricle include:

Easily fatigued, especially during crying spells and at feeding time

Low tolerance for exercise or extra exertion

Shortness of breath (dyspnea) and/or rapid breathing

Fainting (syncope) or collapsing

Difficulty eating, breathing or sucking

Poor weight gain

Slow growth or other physical retardation

Heart murmur, as detected by a physician
In severe cases, the child may also show signs of heart failure, which include the following:

An abnormal heart murmur

A crackling sound of fluid in the lungs (rales), which is a sign of pulmonary congestion

A rapid heartbeat (tachycardia) or abnormal heart rhythms (arrhythmias)

Swelling and fluid retention (edema) in the liver or gastrointestinal tract (in advanced stages of heart failure)

Hypertrophy (muscle thickening) or enlargement of the heart

Liver malfunction

Diagnosis methods for single ventricle

In addition to a patient medical history and a complete physical examination, a physician will generally order one or more of the following tests when diagnosing single ventricle:

Chest x-ray to get an image of the heart's chambers, vessels and muscles. This will also help physicians to see whether there is an overcirculation of oxygen through the lungs, as is often seen with this condition.

Electrocardiogram (EKG) to gauge the electrical activity of the heart.

Echocardiogram to determine the relationships, dimensions, dynamics, and function of all heart chambers, valves, blood vessels, and walls. It also may gauge the direction and speed of blood flow within and around the heart, give some indication of the workload placed on the lungs and check the performance of the heart valves. Both fetal and infant echocardiograms are available. This is usually considered the definitive test to diagnose a single ventricle.

Cardiac catheterization to determine if there are abnormalities present that could not be defined with echocardiography. During the cardiac catheterization, an angiogram may be done, in which a special dye (contrast medium) is injected into the blood vessels to view the activity of vessel walls, valves and the heart muscle. This procedure is usually not required for the initial diagnosis of the condition nor planning the first surgical procedures. It is frequently done in order to plan subsequent surgical procedures.

Blood tests (particularly arterial blood gases) to assess oxygen levels and detect other indicators of illness that may be present in the blood.

Treatment options for single ventricle

The treatment for single ventricle generally involves at least two surgeries performed at separate times in the child’s life. If possible, the first surgery is usually performed at three to six months of age. There are a variety of names for this surgery, which include the following:

Bidirectional Glenn procedure
Glenn shunt operation (or modified Glenn shunt operation)
Glenn anastomosis
Partial Fontan

During this surgery, the superior vena cava (which collects oxygen-poor blood from the upper part of the body) is connected directly to the pulmonary artery (which travels from the single ventricle to the lungs), bypassing the heart. This new pathway allows oxygen-poor blood from the head and upper body to passively flow to the lungs, without getting mixed with oxygen-rich blood in the single ventricle. Once the blood has become enriched with oxygen in the lungs, it goes back to the heart and is pumped out to the body. The interatrial septum (wall between the receiving chambers) is usually removed (atrial septectomy) at this time to allow free mixing of blood within the receiving chambers

This is a crucial step in avoiding the mixing of oxygen-rich and oxygen-poor blood. However, it is only half-finished because the oxygen-poor blood returning from the lower part of the body has not yet been re-routed. At this stage, the baby will still have a bluish tinge, but will be better able to handle infection and other problems.

The second surgery, called the Fontan, is usually performed before the child reaches the age of three, and allows oxygen-poor blood from the upper and lower body to flow directly to the lungs. After this surgery, there is no longer any mixture of oxygen-rich and oxygen-poor blood, and the skin tone should become normal and healthy.

One variation of the Fontan is known as the lateral tunnel Fontan, or a total cavo-pulmonary connection (TCPC). In this procedure, a patch (made of either synthetic materials or the patient's own tissue) is used to create a tunnel within the right atrium. The tunnel links two major veins, the superior vena cava and the inferior vena cava, which are then connected to the pulmonary artery.

A slight variation of the lateral tunnel Fontan is the fenestrated Fontan. In this procedure, a hole is made in the tunnel. This hole allows for decompression of the blood into the right atrium when the pressure within the tunnel gets too high. Later, if the patient has stabilized, the hole can be closed with either a stitch or a catheter procedure. Studies are ongoing toward perfecting computer-imaging techniques that, in turn, can help surgeons plan the best surgical treatment and outcome for each patient.

In rare cases, patients who experience complications during surgery or who are unsuitable candidates for either of the two procedures may undergo a heart transplant. Prognosis and prevention with single ventricle

The treatment for single ventricle has only been available for about 20 years, so long-term prognosis is not yet known. In the short-term, cardiovascular function improves tremendously. However, patients who have undergone surgery for single ventricle are at an increased risk for certain complications such as thrombosis, atrial flutter (a type of arrhythmia) and fluid around the heart (pericardial effusion) or chest (pleural effusion). This may require lifelong monitoring and possibly even medications.

The patient may be advised to avoid certain competitive sports and training that involve short bursts of intense activity (e.g., sprinting, weight-lifting). However, many of these children may participate in aerobic sports such as swimming, running, baseball, soccer, and gymnastics so long as they can set their own pace.

Additionally, antibiotics may be recommended before dental procedures and other surgeries to prevent infection of the heart lining (bacterial endocarditis). Because of an increased risk of clots in the lungs after the hemi-Fontan and Fontan procedures, most of these children receive low dose aspirin on a daily basis, similar to the precautions that adults with coronary artery disease follow. Monitoring the function of the liver and intestines is also necessary as some patients may development a malfunction in their performance. This may require dietary modifications and possibly medications
In addition, children with single ventricle may be required to make changes to their routine infant immunization schedule during the first two years of life. Parents should consult with their pediatrition about what changes should be made.

In the long-term, there have been reports of people experiencing heart failure and even requiring heart transplantation 10 to 20 years after being treated for single ventricle. Therefore, children who have been treated for single ventricle are urged to avoid the risk factors associated with heart failure, which include:

Obesity (body mass index of 30 or greater)
Lack of exercise
Unhealthy dietary habits, such as high salt intake, instead of eating a heart-healthy diet
Alcohol abuse
Abuse of some types of drugs (primarily amphetamines and cocaine)
A severe congenital heart defect of this nature may be corrected but never cured. Therefore, the child will require specialized care with a pediatric cardiologist and, later in life, an adult cardiologist with special training in the care of adult congenital heart disease, for life.

Because the cause of single ventricle is unknown, there are no known strategies to prevent it. However, it has been shown that any type of congenital heart disease in either the mother or father increases the chances of a defect developing in the fetus


About patent ductus arteriosus (PDA)
A patent ductus arteriosus (PDA) is a heart defect that occurs when a blood vessel in the heart called the ductus arteriosus fails to close after birth, as it normally should. The ductus arteriosus is present in every normally developing fetus and is actually is required for the survival of the fetus.

Prior to birth the lungs are collapsed and the fetus receives all its oxygen from the mother. The blood returning to the heart must be detoured away from the lungs. There are two detours present in all fetuses. One connects the two receiving chambers – foramen ovale. The other is the ductus arteriosus.

Closure of either of these prior to birth puts such an increased workload on the fetal heart and circulatory system that survival of the fetus is unlikely. Both of these channels close shortly after birth when the newborn is breathing on his or her own and blood must be pumped directly out to the lungs.
Potential problems that PDA may cause

The size of the patent ductus arteriosus (PDA) determines the severity of the problem. If the PDA is no bigger than the point of a needle, only a small amount of blood can squeeze through the tiny opening. Symptoms for this tiny PDA may be very mild or not even noticeable.

If the PDA is larger than a needlepoint, the child may develop signs and symptoms of heart failure, including poor feeding habits, slow weight gain, constant sweating, labored breathing and a fast heart rate. The increased volume of blood in the lungs may also cause frequent chest colds and pneumonia.

The defect can also lead to endocarditis, an infection that inflames the valves and lining of the heart. If endocarditis develops, the consequences can be life-threatening and irreversible. Endocarditis can occur with a large or small PDA.

If unrepaired, a large PDA can cause damage to the lining of the lung vessels from high blood flow, which can lead to a permanent hardening of the arteries in the lungs. If this occurs, the pressure in the lungs rises, and oxygen-poor blood is forced into the PDA and out to the body. The result is a condition called cyanosis, in which the skin, lips, fingernails and other parts of the body turn a shade of blue from the circulation of oxygen-poor, “blue” blood. This condition is called Eisenmenger syndrome. This condition is very rare in the United States. The arteries and veins in the lungs in patients with Eisenmenger syndrome have permanent scarring that is usually irreversible. This is termed “end-stage” and closure of a PDA is no longer possible.

Heart failure is also associated with untreated PDAs, especially among the very young or in the elderly. Finally, PDA can cause pulmonary hypertension, or increased blood pressure in the lungs. This can eventually lead to vascular (blood vessel) disease. In some cases, a PDA can also cause kidney disease. In very small or very premature newborns a PDA may lead to abnormal blood flow to the intestine resulting in bleeding in the bowel and even loss of the bowel.
Diagnosis methods for PDA

Unlike many congenital heart defects, a PDA cannot be diagnosed in utero because it is a normal feature of a developing fetus. Instead, the condition is diagnosed by the presence of symptoms after birth.

A patent ductus arteriosus (PDA) causes rather forceful blood flow, which makes a sound known as a heart murmur. Listening for this murmur is the most widely used method to screen for heart disease in infants. By listening to the chest with a stethoscope (a procedure called auscultation), the physician may be able to detect a murmur, which begins softly as the heart begins its pumping cycle, and peaks just before and after the second heart “thump.” The murmur is the noise of blood being forced through the PDA.

The murmur of a PDA is often not noted for several weeks after birth because the pressure in the arteries leading to the lungs may be high enough that there may be very little flow through the PDA. As the pressure in the pulmonary arteries drops below that in the aorta the flow through the PDA will increase and the intensity of the murmur becomes more evident.

In addition to listening to the patient's heart, the physician will take the baby’s pulse at birth. The physician may notice a bounding pulse, in which the pulse reaches a higher intensity than normal, then quickly disappears.

When PDA is suspected, a patient may undergo a series of tests such as:

Echocardiogram. This test uses sound waves to visualize the structures and functions of the heart. A moving image of the patient’s beating heart is displayed on a video screen, where a physician can study the heart’s thickness, size and function. The image also shows the motion pattern and structure of the four heart valves, revealing any potential leakage (regurgitation) or narrowing (stenosis). During this test, a Doppler ultrasound may be done to evaluate blood flow through the PDA. This is the definitive test in diagnosing a PDA. It may also help in judging the significance of the defect and whether there are any other associated malformations.

Chest x-ray. A radiation-based imaging test that offers the physician a picture of the general size, shape, and structure of the heart and lungs. This test may show congestion of the lungs because of increased fluid.

Electrocardiogram (EKG). A recording of the heart's electrical activity as a graph on a moving strip of paper or video monitor. The highly sensitive electrocardiograph machine helps detect heart irregularities, disease and damage by measuring the heart's rhythms and electrical impulses. This test is generally normal in the child with a PDA unless the defect is so large that there is considerable, chronic overwork to the pulmonary blood vessels and left ventricle.

Among premature infants, PDA can possibly be detected by such symptoms as troubled breathing, abnormal heart rhythm and other symptoms of heart failure.

Treatment and prevention of PDA

There are a number of methods to treat a patent ductus arteriosus (PDA). Each involves little risk to the life of the patient, and the overall survival rate is 99 percent. The patient’s age and the presence of other congenital heart defects are two of the most important factors that determine how and when the PDA will be repaired.

In a premature baby, a medication called indomethacin may be given to stimulate the ductus arteriosus muscles to contract, thus closing the ductus arteriosus. The medicine works by blocking the effects of prostaglandin. This medicine is usually given in several courses, usually 12 to 24 hours apart. It has a number of possible side effects, however, which include kidney dysfunction and internal bleeding.

Medication is not effective to close the PDA in a full-term infant or older child. In this case, the patient might be given diuretics to reduce blood pressure until their condition is stabilized and a treatment course can be chosen. Two methods are available to close a PDA in these patients: catheter-based procedures and surgery. Catheter-based procedures are not available for preterm infants. In these fragile patients, if indomethacin is unsuccessful or if the medication cannot be employed because of other medical conditions the newborn has, surgical closure is the only means of dealing with a symptomatic PDA.

Catheter-based procedures are techniques in which a catheter is inserted through a blood vessel in the body and guided all the way to the heart, where it can be used by a physician for a number of procedures, including coil embolization. Coil embolization is a relatively new technique that has been adopted by many institutions since it was first implemented for PDA in 1992. It is now one of the most common interventional procedures performed and has been successful in over 95 percent of the cases, although there is a small risk of embolism, or blood clots, during the procedure itself.

Coil embolization uses a coil made of surgical steel in which synthetic fibers are embedded. The coil is delivered via a catheter that is threaded through an artery or vein (e.g., in the groin) to the site of the PDA. Placed inside the PDA, the coil is held in place while the fibers encourage the formation of a blood clot, sealing the PDA closed. Researchers are working on coils that are retrievable so they can be repositioned several times during the procedure to ensure a good fit. These newer coils reduce the risk of embolism caused by the coil itself.

The decision to recommend surgery, in both term and preterm infants, relies on several factors, including the age of the infant and the degree of the opening. Surgery is an acceptable alternative, even among preterm infants, but it is usually not recommended for very small PDAs even if the infant did not respond to indomethacin therapy. Among older infants, a PDA of 1 or 2 mm is not likely to cause any abnormalities in blood flow, but there is a risk that the PDA could be a site for infection of the heart in the future.

During surgery, the infant is given general anesthesia and the surgeon enters the chest through a small incision under the left arm (thoracotomy). One in the chest, the surgeon ties off the ductus arteriosus between the aorta and the pulmonary artery. Less than 1 percent of these blood vessels reopen, making this technique among the most reliable procedures.

Surgery is usually reserved only for symptomatic newborns who require a ventilator to support their breathing. The extra work on the heart and lungs because of a PDA may interfere with the newborn’s ability to breath without the machine. Closure of a PDA in this setting may allow the newborn to breath without the ventilator. There are several possible complications from surgery that are not present with device closure.

Another type of surgery, called video-assisted thoracoscopic surgery (VATS), involves the use of specialized long instruments, which are inserted through small puncture holes in the chest to close PDAs. This does not require spreading of the ribs which shortens the recovery time. The instruments place a metal clip around the PDAs, which seals the defect.

Although its cause is unknown and it cannot be prevented, PDA occurs much more commonly in premature and very low birth-weight (VLBW) infants. Infants are also at much greater risk if the mother contracts rubella (German measles) near the time of birth. Fortunately rubella is rarely seen in this country because of routine vaccination. Pregnant women are also routinely checked for immunity to rubella, usually on their first obstetrical visit along with several other blood tests.

The ductus arteriosus is considered patent (open) if it does not seal itself within three days after the baby is born.

A large patent ductus arteriosus results in a left-to-right shunt, causing blood to move across the open blood vessel from the left side of the heart (aorta) to the right (pulmonary artery). This raises blood pressure in the pulmonary circulation and increases work on the right ventricle. At the same time, there is increased pulmonary return to the left side of the heart (because of the increased blood volume in the right side of the heart), which adds additional stress on the left side of the heart. This can result in an expanded left atrium and ventricle. If the degree of patency (openness) is large enough, it can eventually cause pulmonary vascular disease, as well as symptoms associated with heart failure because the heart is unable to pump enough oxygen-rich blood to satisfy the body.

Although a PDA is often harmful to the baby, there are times when a PDA can be helpful (e.g., tetralogy of Fallot) because it establishes some semblance of normal blood flow. When other heart defects are present, a PDA may serve a crucial and life-sustaining function. In patients with blockage of blood flow to the lungs, for example, a PDA allows blood to flow to the baby’s lungs. Similarly, among babies born with complex congenital heart defects with abnormal circulation, a PDA may enable the baby to live by mixing oxygen-rich and oxygen-poor blood.

One such abnormality is transposition of the great arteries, in which the positions of the aorta and pulmonary artery are reversed, resulting in two sets of parallel circulation. Without a PDA or some way for blood to cross the septal barrier, the baby would rapidly die. In some cases, physicians may administer a special drug called prostaglandin E1 that will keep the ductus arteriosus open long enough to allow such a baby to get into surgery.

About 35,000 babies are born every year with heart defects, according to the American Heart Association. A PDA is one of the 10 most common heart defects in the United States. Premature babies are most at risk for the condition. Other risk factors include maternal rubella (German measles) during pregnancy, birth in a city or town at high altitude, and a family history of PDA.
Role of the ductus arteriosus

During fetal development, the lungs are not yet functioning, and the fetus relies on the mother to supply it with fresh, oxygen-rich blood through the umbilical cord. Although the pulmonary artery will carry oxygen-poor blood to the lungs after birth, there is no reason for blood to go to the lungs before birth for two reasons. First, the fetal blood already contains oxygen from the placenta and second, the fetal lungs will not contain any oxygen from the air. Therefore, the pulmonary artery carries blood that is rich in oxygen from the placenta through the ductus arteriosus and to the aorta, which funnels the blood to the rest of the fetus’ body.

After birth, there are several factors that must occur to close the ductus. First, during pregnancy, the vessel is held open by circulating prostaglandin, a hormone-like fatty acid that helps control smooth muscle contraction. After birth, the level of prostaglandin in the blood declines and there is an increased level of vasoconstrictive substances. At the same time, there is an increased pressure with the ductus arteriosus itself due to the presence of oxygen in the blood after the baby takes its first breath. As a result, the ductus arteriosus typically closes within the first 24 hours after birth.

Within two to three days, a scar forms over the site of the ductus, sealing it permanently. The pulmonary artery now works to bring oxygen-poor blood from the right ventricle to the lungs, where the blood can receive a fresh supply of oxygen from the inhaled air.

If it remains open, then it is known as a patent ductus arteriosus (PDA) and is considered a congenital heart defect. This is a problem because of the way the normal, mature heart operates. In a normal heart, the pressure is greater in the left side of the heart. Thus, in a heart with a PDA, blood is pushed from the left side of the heart back into the right side of the heart. This raises the blood volume in the pulmonary artery and lungs, while also decreasing the amount of oxygen-rich blood flowing to the body. Over time, this can result in pulmonary disease (e.g., pulmonary hypertension), kidney disease, and left-sided heart failure.


Situs inversus (also called situs transversus) is a rare congenital condition in which the major visceral organs are reversed or mirrored from their normal positions. The normal arrangement is known as situs solitus. In other rare cases, in a condition known as situs ambiguus or heterotaxy, situs cannot be determined.
The term situs inversus is a short form of the Latin phrase "situs inversus viscerum," meaning "inverted position of the internal organs." Dextrocardia (the heart being located on the right side of the thorax) was first recognised by Marco Severino in 1643. However, situs inversus was first described more than a century later by Matthew Baillie.
The prevalence of situs inversus varies among different populations but is less than 1 in 10,000 people.[1]


Situs inversus causes the positions of the heart and lungs to be mirrored.
The condition affects all major structures within the thorax and abdomen. Generally, the organs are simply transposed through the sagittal plane.
The heart is located on the right side of the thorax, the stomach and spleen on the right side of the abdomen and the liver and gall bladder on the left side.
The left lung is trilobed and the right lung bilobed, and blood vessels, nerves, lymphatics and the intestines are also transposed.
If the heart is swapped to the right side of the thorax, it is known as situs inversus with dextrocardia or situs inversus totalis.
If the heart remains in the normal left side of the thorax, a much rarer condition (1 in 22,000 cases of situs inversus), it is known as situs inversus with levocardia or situs inversus incompletus.
Situs inversus with levocardia, or dextrocardia without situs inversus, present much higher rates of congenital defects than situs inversus with dextrocardia.


Situs inversus is generally an autosomal recessive genetic condition, although it can be X-linked or found in identical "mirror" twins.[2]
In the absence of congenital heart defects, individuals with situs inversus are phenotypically unimpaired, and can lead normal healthy lives, without any complications related to their medical condition.
There is a 5-10% prevalence of congenital heart disease in individuals with situs inversus totalis, most commonly transposition of the great vessels. The incidence of congenital heart disease is 95% in situs inversus with levocardia.
Many people with situs inversus are unaware of their unusual anatomy until they seek medical attention for an unrelated condition. The reversal of the organs may then lead to some confusion, as many signs and symptoms will be on the 'wrong' side.
For example, if an individual with situs inversus develops appendicitis, they will present to the physician with left lower abdominal pain, since that is where their appendix lies. Thus, in the event of a medical problem, the knowledge that the individual has situs inversus can expedite diagnosis. People with this rare condition should inform their physicians before an examination, so they may redirect their search for heart sounds and other signs.
Situs inversus also complicates organ transplantation operations as donor organs will almost certainly come from situs solitus donors. As hearts and livers are chiral, geometric problems arise placing an organ into a cavity shaped in the mirror image.
For example, a person with situs inversus who requires a heart transplant needs all the vessels to the transplant donor heart reattached to their existing ones. However, the orientation of these vessels in a person with situs inversus is reversed, necessitating steps so that the blood vessels join properly.

Kartagener syndrome

Situs inversus is generally inherited in an autosomal recessive pattern.
Further information: primary ciliary dyskinesia
About 25% of individuals with situs inversus have an underlying condition known as primary ciliary dyskinesia (PCD).
PCD is a dysfunction of the cilia that manifests itself during the embryologic phase of development.
Normally-functioning cilia determine the position of the internal organs during early embryological development, and so individuals with PCD have a 50% chance of developing situs inversus.
If they do, they are said to have Kartagener syndrome, characterized by the triad of situs inversus, chronic sinusitis, and bronchiectasis.
Cilia are also responsible for clearing mucus from the lung, and the dysfunction causes increased susceptibility to lung infections.
Male sufferers of PCD are often infertile: the cilia that make up the tail of individual sperm cells are also defective, thus rendering the sperm ineffective.

Tuesday, March 16, 2010

Dah cuti sekolah....

Assalamualaikum....dah lam tak menjengah blog nih....pasai pa...senarnya pasai poli nih lah....server tak membenarkan...kalu buka email poli kejap jer dai boleh capai...kalu nak masuk fb kita ker....buka pagi tengahari nanti baru boleh achieve...tu yang maleh nak buka blog nih...kat umah almaklumlah....tak sempatnye...cuti sekolah dah mula...makna kata cuti poli pon sama...tapi nasib kami tak sama...kami kena keje gak.....hari jumaat lepas sempat juga balik alor setar...tapi kita balik ngan anak2 jer....hubby ader klas hari sabtu...adik yang bawah kita datang amik...sian dengaor kakak nak balik naik bas....

amboi...udah siap umah tok walid ngan maktok...besar nyer...adik kata cantiknyer....maklumlah lah tak lama lagi maktok ngan tok walid nak terima manantu baru...dibuatnya umah besar senang sedara mara nak berkampung kat sini...abang ngan adik balik umah tok walid tarin panjang lah...semua kehendak akan disempurnakan oleh mak tok, tok walid, aunty eda, auty eja dan pak su...lemak la baby lak..dah tak mo kat sesaper kecuali taok walid...tu lah jarang balik...sampai baby tak mo kat kita kat sana 3 hari...kita amik cuti dua hari...ahad dah balik kulim...isnin lepak kat umha....hari nih dah keje...tak dok orang pon...kebanyakan nyer semu cuti...berjalan....

emmmm...sebut pasal baby nih...sekarang nih dia tengah mabuk nak jalan..tapi kaki tu belum kuat lagi...keje jatuh jer...sian plak...semalam dah jatuh katil...lekt bekas kat muka...sian dia...hari tu dih gi ijn...kita dah booking tarikh nak masukkan kamera dalambadan dia...tarikh kena admit 6/10/2010...hari nak buat tu 7/10/2010...doktor kata kalu tak der aper2 hal hari 8/10/2010 dah boleh kuar...insyalllah...doa2kan lah kesihatan dia...sekang nih berat faris dah tak mo naik cam dulu...buas sama...keje nak main jer....dan bila dia main nampak sangat dia penat...apa nak kata memang budak cam tu lah keje nak untuk follow up yang seterusnya bulan 6 pla....25/6/2010...yg tu yang biasa 3 bulan sekali...buat masa skang nih...kesihatan faris maintain....alhamdulilah takat nih sajer nak berceloteh...nanti2 kita report lagi...key...sampai jumpa lagi...