Warung Bebas

Friday, 30 September 2011

Nasopharyngeal Carcinoma Therapy

Hello Mbah Dukun Bagong, modern shaman comes again. today mbah dukun will explains about how to therapy the cancer of nasopharyngeal, following last post. There are 2 therapies for this disease. what are they? okey check it out

A. Primary Therapy

1. radiotherapy

Until recently, radiotherapy still plays an important role in the management of nasopharyngeal carcinoma. Management of nasopharyngeal carcinoma is the first to radiotherapy with or without chemotherapy.
2. chemotherapy
Chemotherapy as an adjunct therapy in nasopharyngeal carcinoma was found to improve therapeutic outcomes. Especially, given the advanced stage or on the state of relapse.
Various combinations are developed, the best to date is combined with Cis-platinum as the core
Giving chemotherapy anjuvan Cis-platinum, bleomycin and 5-fluororacil with interim results that are satisfactory. Similarly, studies have been conducted of chemotherapy praradiasi with epirubicin and cis-platinum, although there are side effects severe enough, but it gives hope of a better cure.
3. operation
Surgery in patients with nasopharyngeal carcinoma are, radical neck dissection and nasopharyngectomy. Neck dissection is performed if there is still residual gland after radiation or a recurrence of the gland with the proviso that the primary tumor has been cleared as evidenced by radiological examination and serology. Nasopharyngectomy is a palliative operation is performed in relapse cases or the presence of residues that are not successful in the nasopharynx treated by other ways.
4. immunotherapy
By knowing the possible causes of nasopharyngeal carcinoma is the Epstein-Barr virus, So patients can be administered immunotherapy.

Radiotherapy is a method of treatment of malignant diseases using lawyer-ion beam, aiming to kill tumor cells as much as possible and maintain the healthy tissue around the tumor so as not to suffer the damage is too severe. Nasopharyngeal carcinoma is radioresponsif that radiotherapy remains an important therapy.
Radiation on tissue, can cause ionization of water and electrolytes from the body fluids both intra-and extra-cellular, so that the resulting very reactive H + and OH-. Ions that can react with a molecule of DNA in the chromosomes, so
can occur:
1. DNA double chain break
2. Changes in cross-linkage in the DNA chain
3. Base changes that cause degeneration or cell death.
Lethal dose and the ability to repair damage to cancer cells is lower than normal cells, so the effect of radiation, the cancer cells more likely to die and remain damaged compared with normal cells.
The cells that still survive, will hold its DNA damage repair on their own. DNA repair ability of normal cells better and faster than the cancer cells. This situation is used as a basis for radiotherapy in cancer.
At the VIII International Congress of Radiology in 1953, set RAD (radiation absorbed Dose) as the amount of energy absorbed per unit of tissue. Currently the International System units (SI) of dose on absorption has been changed to Gray (Gy) and the unit often used is the unit of centi gray
1 Gy = 100 rad
1 rad = 1 cGy = 10-2 Gy.,
Treatment outcomes are expressed in numbers in response to irradiation is highly dependent on tumor stage. The more advanced tumor stage, the less response. For stage I and II, obtained a complete response 80% - 100% with radiation therapy. Whereas stage III and IV, found the numbers
failure of local response and distant metastases is high, namely 50% - 80%. Survival rate of patients with nasopharyngeal carcinoma depends on several factors, foremost among which is the stage of disease.
a.    Preparation / planning prior to radiotherapy
Before, were given radiation therapy, clinical staging was made, histopathologic diagnosis, as well as determined the purpose of radiation, curative or palliative. Patients also prepared mentally and physically. To the patient, if necessary, the family also provided information regarding the necessity of this action, the purpose of treatment, side effects that may arise during the treatment period.
Physical examination and laboratory before starting radiation is absolute. Patients with poor general condition, malnutrition or fever are not allowed to radiation, except in patients with life-threatening circumstances, such as track digestivum obstruction, massive bleeding from the tumor, radiation still starts while improving the general state of the patient. As a benchmark, Hb levels should not be less than 10 g%, the number of leukocytes can not be less than 3000 per mm3 and platelets 100,000 per uL.
b. Determination of the limits of the radiation field
This action is one of the most important step to ensure the success of the radiotherapy. Radiation field included the primary tumor and the surrounding area / potential to continue spreading and lymph-regional lymph nodes.For tumor stage I and II, the following areas should be illuminated:
1. The entire nasopharynx
2. The entire base of the sphenoid and occiput
3. cavernosal sinuses
4. Cranial base, a minimum width 7 cm 2 covering the foramen ovale, carotid canal and jugular foramen laterally.
5. Rear half of nasal cavity
6. Posterior Etmoid sinus
7. 1 / 3 posterior orbit
8. 1 / 3 posterior maxillary sinus
9. fossa pterygoidea
10. Lateral and posterior pharyngeal wall as high as midtonsilar fossa
11. gland retrofaringeal
12. Bilateral cervical glands including the posterior jugular, spinal accessory and supraclavicular
If there is an extension to the nasal cavity or oropharynx (T3) the entire cavity and oropharynx nasal should be included in the radiation field. If the extension through the skull base has reached the cranial cavity, the upper limit of the radiation field is located above the pituitary fossa. If the spread of tumor to the maxillary sinus and Etmoid or orbit, around the sinuses or the orbit should be irradiated. Submental and occipital lymph nodes are not routinely included, unless a massive cervical lymphadenopathy was found or if there is metastasis to the sub-maxillary glands.
irradiation field boundaries are:
- Superior: covering the cranial base, sella tursika included in the radiation field.
- Anterior: located behind the eyeball and choana
- Posterior: right behind the external acoustic meatus, except when there is enlargement of the gland the rear boundary should be located 1 cm beyond the palpable glands.
- Inferior: located on the top edge of thyroid cartilage, these limits change when obtained enlarged neck glands, which is 1 cm lower than the gland is palpable. This field of radiation received from the left and right of the patient.
In patients with neck glands are very large so that the radiation in the above methods can not be done, then the radiation field is given by the front and rear.
The upper limit includes all the cranial base. The lower limit is the bottom edge of the clavicle, the left and right limits are 2 / 3 of the distal clavicle, or follow the magnitude of the gland.
Gland supra clavicle and lower neck received radiation from the field in front, the upper limit of the radiation field is coincident with the lower limit of the radiation field to the primary tumor.
c.    Rays to radiotherapy
Rays used for radiotherapy are:
1. Alpha rays
Alpha rays are corpuscular rays or particles from the nucleus. The nucleus consists of protons and neutrons. This light can not penetrate the skin and are not widely used in radiotherapy.
2. Beta rays
Beta rays is the electron ray. These rays emitted by radioactive substances that have low energy. Power breakdown of the skin is limited, 3-5 mm. Used for the treatment of superficial lesions.
3. Gamma rays
Gamma rays are electromagnetic rays or photons. These rays can penetrate the body. Depending on the power breakdown of the energy that causes the beam. The higher energy or higher voltagenya, the bigger and more power breakdown in the location of the maximum dose.
d.     radioisotopes
1. Caecium137! gamma rays
2. Cobalt60! gamma rays
3. Radium226! alpha rays, beta, gamma.
e. Radiotherapy technique
There are three main ways of radiotherapy, namely:
1. External radiation / teletherapy
Ray sources in the form of X-ray apparatus or a radioisotope which is placed outside the body. Beam is directed into the tumor to be given radiation. Much energy is absorbed by a tumor depends on:
a. The amount of energy emitted by energy source
b. The distance between the source of energy and the tumor
c. Density of the tumor mass.
Teletherapy fractional generally administered at a dose of 150-250 rad per time, in 2-3 series. Among the series 1-2 or 2-3 given 1-2 weeks to break the person's condition so that recovery takes 4-6 weeks of radiotherapy.
e.    2. International Radiation / Brachytherapy
Energy source is placed inside the tumor or adjacent to the tumor in the body cavity. There are several types of internal radiation:
a. interstitial
Radioisotopes in the form of needle inserted into the tumor, for example, radium needles or needle irridium.
b. Intracavitair
The provision of radiation can be done by:
- After loading
An empty applicator is inserted into the body cavity to
the tumor. After the applicator is located right, enter new
radioisotope into the applicator.
- Installation
Radioisotope solution injected into the body cavity, for example:
pleura or peritoneum.
3. intravenous
Radioisotope solution injected into a vein. For example, I131 is injected IV will be absorbed by the thyroid to treat thyroid cancer.
f.    radiation dose
There are two types of radiation, namely:
1. Curative radiation
Awarded to all levels of disease, except in patients with distant metastases. Target of radiation is the primary tumor, lymph nodes of the neck and supra clavicle. Total radiation dose given was 6600-7000 rad to 200 rad fractions, 5 x delivery per week. After a dose of 4000 rad to the spinal cord in the block and after 5000 rad irradiation supraclavicular field were excluded.
2. Palliative radiation
Given for metastatic tumors in bone and local recurrence. The dose of radiation to bone metastases with 3000 rad 300 rad fractions, 5 x per week. For local recurrence, radiation field is limited to local relapse.
g. radiation response
After the radiation is given, then the evaluation of response to radiation. Assessed the response of cervical lymph node reduction and downsizing of the primary tumor in the nasopharynx. Assessment of radiation response based on WHO criteria:
- Complete Response: remove all the lymph nodes are large.
- Partial Response: downsizing of the lymph nodes to 50% or more.
- No Change: the size of lymph nodes that persist.
- Progressive Disease: size of enlarged lymph nodes of 25% or
h. complications of radiotherapy
Complications of radiotherapy can be:
1. early complications
Usually occur during or several weeks after radiotherapy, such as:
- Xerostomia - Nausea, vomiting
- Mukositis - anorexia
- dermatitis
- Erythema
2. further complication
Usually occurs after 1 year of radiotherapy, such as:
- Contractures
- Impaired growth
- etc.

B. Palliative care
Palliative care is any active measures to ease the burden of cancer patients especially those that can not be cured. Said to be mainly on the unlikely cure because these actions are not only performed on patients who can not be cured but it worked well in patients who still have hope of recovery together - together with the action - the action or curative treatment, with a view to alleviate or eliminate symptoms - symptoms that disrupt or even aggravate the suffering of patients.

Active measures in question are, among others, relieve pain and complaints - other complaints, improvements in aspects of psychology, social and spiritual. All this aims to improve the quality of life is maximized, for patients and families.
The first attention should be given to patients with radiation treatment. Mouth dryness is caused by damage to major or minor salivary glands during irradiation. Not much can be done in addition to advise patients to eat with lots of sauce, bring drinks to go anywhere and try to eat and chew the material so that the sour taste stimulates saliva. Other disorders of the oral cavity is mukositis because mushrooms, stiffness in the neck because fibrotic tissue caused by irradiation, headache, loss of appetite and sometimes vomiting or nausea.

Difficulties arising in the care of patients post-treatment where the tumor remains incomplete (residual) or relapse (residif). Can also arise post-treatment metastatic far as to bone, lung, liver, brain. In the second condition mentioned above is not much action that can be given medical treatment other than simtimatis to improve the quality of life of patients. The patient eventually died of poor general condition, bleeding from the nose and nasopharynx that can not be stopped and the undermining of vital equipment due to tumor metastasis.

Thursday, 29 September 2011

Nasopharyngeal Carcinoma (Nasopharyngeal Cancer)

Be carefull if you smoke ciggaret and eat saltfish too much, because they make deadly disease called Nasopharyngeal Carcinoma or Nasopharyngeal Cancer. Today Mbah Dukun Bagong, Indonesian Modern Shaman special author from Medical and Health Information explains about this cancer. wish it is so usefull for us.

Carcinoma or cancer is a malignant growth of new cells, composed of epithelial cells that tend to infiltrate surrounding tissues and cause metastases.
Nasopharyngeal carcinoma is a malignant tumor arising in the epithelial coating the space behind the nose (nasopharynx).

The link between Epstein-Barr virus and the consumption of salted fish said to be the main cause of this disease. Epstein-Barr virus can enter the body and remain there without causing an abnormality in a long time. To activate this virus requires a mediator. The habit of eating salted fish are constantly starting from childhood, is the main mediator that can activate the virus causing nasopharyngeal carcinoma.
Mediator below are considered influential to the onset of carcinoma
nasopharyngeal namely:
1. Salted fish, preserved foods and nitrosamines.
2. State of low socio-economic, environmental and lifestyle habits.
3. Frequent contact with substances that are considered carcinogens, such as:
- benzopyrenen
- benzoanthracene
- Chemical gases
- Industrial smoke
- Wood smoke
- Some plant extracts
4. Race and ancestry
5. Chronic inflammation of the nasopharynx
6. HLA profile

 Saltfish causes nasopharyngeal carcinoma

Microscopically, nasopharyngeal carcinoma can be divided into three forms, namely:
1. ulcerative forms
This form is most often found on the posterior wall and the area around the fossa rosenmulleri. Can also be found on the lateral wall in front of the tube and on the roof eustachius nasopharynx. These lesions are usually accompanied by smaller necrotic tissue and is very easy to conduct infiltration into surrounding tissue. Histopathologic picture is a form of squamous cell carcinoma with good differentiation.
2. nodular / lubuler / proliferative forms
Nodular form or lobuler very often found in the area around the estuary eustachius tube. This type of tumor shaped like grapes or polypoid rarely, found the existence of ulceration, but is sometimes found a small ulceration. Histopathologic picture of carcinoma usually without differentiation.
3. exophytic forms
exophytic forms usually grow on one side of the nasopharynx, found no presence of ulceration, stemmed and sometimes slippery surface. This type of tumor usually grows from the roof of the nasopharynx and can fill the entire cavity of the nasopharynx. These tumors can encourage the palate mole down and coana grow toward and into the nasal cavity. Histopathologic picture is a limphosarcoma
Nasopharyngeal Cancer
Nasopharyngeal Carcinoma
Nasopharyngeal Cancer
Classification of histopathologic picture of Nasopharyngeal cancer recommended by the Organization
World Health Organization (WHO) before the year 1991, divided into three types, namely:
1. Keratinizing Squamous Cell Carcinoma.
This type of differentiation can be subdivided into good, moderate and bad.
2. Non-keratinizing carcinoma.
In this type of differentiation is found, but no cell differentiation
Squamous intersel without bridges. In general, the cell boundary is quite clear.
3. Undifferentiated carcinoma.
In this type of individual tumor cells showed a vesicular nucleus,
oval or round with a clear nukleoli. Generally, the cell boundaries are not clearly visible.
Types without differentiation and without keratinization typically have the same are radiosensitive. While the type with keratinization is not so radiosensitive.
Histopathological picture of the latest classification recommended by WHO
in 1991, just divided into two types, namely:
1. Keratinizing Squamous Cell Carcinoma.
2. Non-keratinizing carcinoma.
This type can be subdivided into differentiated and not differentiated.

The main symptoms are:
1. Nasal sign:
· Colds that do not heal
· Epistaxis. Blood discharge is usually over and over again, few in number and often mixed with mucus, so it appears pink · Snot may like pus, watery or thick and smelly.
2. Ear sign:
· Tinnitus. Suppress tumor eustachii estuary causing tubal tubal occlusion, because the tube eustachii estuary, close to the fossa rosenmulleri. The pressure in the tympanic cavity is lowered, resulting in tinnitus.
· Conductive hearing loss
· Discomfort in the ear until the ear pain (otalgia).
3. Eye sign:
· Diplopia. Tumor crept laseratum foramen and cause disruption N. IV and N. VI. When exposed Chiasma optic would cause blindness.
4. Tumour sign:
Enlarged neck glands lymphoid · this is the spread or metastases near the lymphogen of nasopharyngeal carcinoma.
5. cranial sign
Cranial symptoms occur when the tumor has spread to the brain and is felt in people. These symptoms include:
· Constant headaches, pain is a metastasis in
· Sensitibilitas of Regional cheeks and nose reduced.
· Difficulty on swallowing
· Aphonia
· Syndrome or syndrome reptroparotidean jugular Jackson on N. IX, N. X,
N. XI, N. XII. With signs of paralysis on:
o tongue
o palate
o Pharynx or larynx
o M. sternocleidomastoideus
o M. trapezeus

1) Epstein-Barr Virus
Epstein-Barr virus replicate in epithelial cells and becomes latent in B lymphocytes Epstein-Barr virus infection occurs in two main places of salivary gland epithelial cells and lymphocytes. EBV infection of B lymphocytes initiate by binding to virus receptors, namely the complement component C3d (CD21 or CR2). Glycoprotein (gp350/220) to the capsule EBV binds to the CD21 protein on the surface of lymphocytes B3.
This activity is a series of chain starting from the entry of EBV into B lymphocytes and subsequent DNA causes B lymphocytes to be immortal. In the meantime, until now the mechanism of EBV entry into nasopharyngeal epithelial cells can not be explained with certainty. However, there are two receptors are thought to play a role in entry of EBV into epithelial cells of the nasopharynx and PIGR CR2 (Polimeric Immunogloblin Receptor). Cells infected by Epstein-Barr virus can cause several possibilities, namely: cell to die when infected with Epstein-Barr virus and virus replication conduct, or Epstein-Barr virus that can lead to cell death meninfeksi virus so that the cells return to normal or transformation can occur namely cell interactions between cells and viruses that result in changes in properties of the cell resulting in cell transformation into malignant cancer cells forming.
EBV genes expressed in patients with Nasopharyngeal Carcinoma is a latent gene, namely Ebers, EBNA1, LMP1, LMP2A and LMP2B. EBNA1 protein plays a role in maintaining the virus in latent infection. Transmembrane protein LMP2A and LMP2B inhibits tyrosine kinase signaling that is believed to inhibit viral lytic cycle. Among those genes, genes that were most responsible for cell transformation is the LMP1 gene. structure
LMP1 protein consists of 368 amino acids that is divided into 20 amino acids at the N terminus, six transmembrane protein segments (166 amino acids) and 200 amino acids at the carboxy end (C). LMP1 transmembrane protein mediates the signal for TNF (tumor necrosis factor) and improve the regulatory cytokine IL-10 which memproliferasi B cells and inhibit the local immune response.
2) Genetic
Although nasopharyngeal carcinoma tumor does not include genetic, but susceptibility to nasopharyngeal carcinoma in a particular community group has a relatively prominent and familial aggregation. Correlation analysis showed HLA (human leukocyte antigen) and cytochrome P450 enzyme gene pengode 2E1 (CYP2E1) is the possibility of gene susceptibility to nasopharyngeal carcinoma. Cytochrome P450 2E1 is responsible for metabolic activation of nitrosamines and related carcinogens.
3) Environmental factors
A large number of case studies conducted in populations residing in different regions in asia and north america, has confirmed that the fish sauce and other foods that contain large amounts of preserved nitrosodimethyamine (NDMA), Nitrospurrolidene (NPYR) and nitrospiperidine (NPIP), which may be a factor carcinogenic nasopharyngeal carcinoma. Also smoking and exposure to secondhand smoke who smoke cigarettes that contain formaldehyde and wood dust tepapar recognized risk factors for nasopharyngeal carcinoma by means of reactivating EBV infection.

1. adenoid hyperplasia
Usually found in children, rare in adults, in children
hyperplasia occurs Because repeated infections. On the plain will be seen a mass of soft tissue on the upper side of the nasopharynx generally demarcated and generally symmetrical and surrounding structures did not appear the signs look bleak infiltration in carcinoma.
2. Angiofibroma juenilis
Usually found in relatively young age with symptoms resembling nasopharyngeal carcinoma. The tumor is rich in blood vessels and the bias is not infiltrative. On the plain will get a mass on the roof nasofairng demarcated. The process can be extended seperrti on the spread of carcinoma, although rarely cause bone destruction
erosion simply because tumor suppression. Usually there is bending toward the front of the rear wall of the maxillary sinus is known as the antral sign. Because these tumors are rich in the vascular external carotid arteriography is necessary because the picture is very characteristic. Sometimes it is also hard to distinguish angiofibroma juvenils with nasal polyps on the plain.
3. Sinus tumors sphenooidalis
Primary malignant tumors sphenoidalis sinus is extremely rare and usually the tumor had reached somewhat advanced stage when the patient came to the first examination.
4. neurofibroma
Group of these tumors often arise in the lateral pharyngeal space that resembles a malignancy in the lateral wall of the nasopharynx. the C.T. Scan, pendesakan space medially toward the pharynx can help distinguish this group of tumors with nasopharyngeal carcinoma.
5.  parotid gland tumor
Parotid gland tumors, especially those from the lobe that lies somewhat in the space of the pharynx and protruding towards the lumen of the nasopharynx. in most cases seen pendesakan parafaring space medial direction that appears on CT scan examination.
6. Chordoma
Although Chordoma is a major sign of bone destruction, but in view of nasopharyngeal carcinoma
too often cause bone destruction, it is often made ​​it difficult to
membedakanya. With a plain, visible calcification or destruction, especially in the clivus region. CT can help to see if there is enlargement of the upper cervical glands because Chordoma typically do not pay attention to an abnormality in the gland, while nasopharyngeal carcinoma frequently metastasize to lymph nodes.
7. Menigioma cranial base
Although these tumors are somewhat rare, but the picture is sometimes resemble
nasopharyngeal carcinoma with sclerotic signs in the area of ​​the cranial base. CT picture of meningioma is quite characteristic that is a bit hyperdense before injecting a contrast agent and will
become very hyperdense after administration of intravenous contrast agent. Arteriography examination also greatly aid in the diagnosis of this tumor.

Most recent staging based on an agreement between the UICC (Union
Internationale Contre Cancer) in 1992 are as follows:
T = Tumor, describes the state of the primary tumor, large and expansion.
T0: No visible tumor
T1: Tumor limited to one location in the nasopharynx
T2: Tumor extends more than one location, but still inside the cavity of the nasopharynx
T3: Tumor extends into the nasal cavity and / or oropharynx
T4: Tumor extends to the skull and / have about the brain's nerve
N = nodule, described the state of regional lymph nodes
N0: No enlargement of the gland
N1: There homolateral gland enlargement can still be driven
N2: There is enlargement of the gland contralateral / bilateral still be driven
N3: There is enlargement of both glands homolateral, contralateral or bilateral, which already
attached to the surrounding tissue.
M = metastases, distant metastases describe
M0: No distant metastasis
M1: There is distant metastasis.
Based on the above TNM, stage of disease can be determined:
Stage I: T1 N0 M0
Stage II: T2 N0 M0
Stage III: T3 N0 M0
T1, T2, T3 N1 M0
Stage IV: T4 N0, N1 M0
Any T N2, N3 M0
Any T Any N M12
According to the American Joint Cancer Committee in 1988, staging of tumors
nasopharynx are classified as follows:
Tis: Carcinoma in situ
T1: The tumor is found on one side of the nasopharynx or tumor that can not be seen, but
can only be known from the biopsy results.
T2: The tumor that attacks the two places, the wall of the postero-superior and lateral walls.
T3: tumor extension up into the nasal cavity or oropharynx.
T4: The tumor that spread to invade the skull or cranial nerves (or both).

Overall, the 5-year survival rate was 45%. Prognosis is worsened by
several factors, such as:
· Stadium further.
Age of more than 40 years
· Men than women
· China than in whites
The enlargement of the gland neck ·
· Existence of damage to brain nerve palsy skull
· Presence of distant metastases

1. Petrosphenoid syndrome
The tumor grows upward into the base of the skull through the foramen laserum until sinus
cavernosal nerves pressing N. III, N. IV, N. VI also suppress N.II. which gives abnormalities:
· Trigeminal neuralgia (N. V): Trigeminal neuralgia is a pain in the
sesisi face marked with flavors such as exposed electrical flow is limited
on the distribution of the trigeminal nerve.
· Ptosis palpebra (N. III)
· Ophthalmoplegia (N. III, IV N., N. VI)
2. Retroparidean syndrome
The tumor grows forward toward the nasal cavity can then infiltrate into the surrounding. Tumor to the side and back toward the area where there retropharing parapharing and lymph nodes. The tumor is pressing against a nerve N. IX, N. X, N.
XI, N. XII with the manifestation of symptoms:
· N. IX: difficulty swallowing because of hemiparesis and the superior constrictor muscle
Taste disturbance at the rear third of the tongue
· N. X: hyper / hipoanestesi moles palate mucosa, pharynx and larynx with
respiratory disorders and salivary
° N XI: paralysis / atrophy bibs trapezius, SCM muscles as well as the palate hemiparese
· N. XII: hemiparalisis and atrophy of the tongue side.
· Horner's syndrome: paralysis of the N. simpaticus servicalis, a narrowing of the fissure palpebralis, onoftalmus and miosis.
3. Cancer cells can contribute to flow with the lymph nodes or blood, the organ that is located far from the nasopharynx. That often is the bones, liver and lungs. This is the end result and a poor prognosis. In another study found that nasopharyngeal carcinoma metastases can hold a lot, to lung and bone,
20% respectively, whereas the liver 10%, 4% of the brain, kidney 0.4%, 0.4% for the thyroid.

Sunday, 25 September 2011

Heterochromia Iridium

Have you ever seen cats, dogs or even people whoose different eye colors? Or never see the character Yuna (Final Fantasy X, in which one side, the color of his eyes is different from the other side?. Now, Mbah Dukun Bagong, the modern shaman form medical and health information will explain of this eye abnormalities.

Heterochromia is a color difference on the individual, such as the eyes, skin and hair. Heterochromia of the eye called Heterochromia Iridium. So Heterochromia Iridium is a condition in which there are differences in the color of the iris in one eye (partial) or both eyes (complete).

Partial Heterochromia Iridium

Complete Heterochromia Iridium

Classification and Etiology
Heterochromia is classified primarily by onset: as either genetic or acquired. Although a distinction is frequently made the between Heterochromia That affects an eye completely or only partially (sectoral Heterochromia), it is Often classified as either genetic (due to mosaicism or congenital) or acquired, with mention as to whether the affected iris or portion of the iris is darker or lighter.

Congenital Heterochromia
Heterochromia That is congenital is usually inherited as an autosomal dominant trait.
Abnormal iris darker
• Lisch nodules - iris hamartomas seen in neurofibromatosis.
• Ocular melanosis - a condition characterized by Increased pigmentation of the uveal tract, episclera, and anterior chamber angle.
• Oculodermal melanocytosis (nevus of Ota)
• Pigment dispersion syndrome - a condition characterized by loss of pigmentation from the posterior iris surface and the which is disseminated intraocularly Deposited on Various intraocular structures, including the anterior surface of the iris.
• Sturge-Weber syndrome - a syndrome characterized by a port-wine stain nevus in the distribution of the trigeminal nerve, ipsilateral leptomeningeal angiomas (leptomaningiomas) with intracranial calcification and neurologic signs, and angioma of the choroid, Often with secondary glaucoma.
Abnormal iris lighter
• Simple Heterochromia - a rare condition characterized by the absence of other ocular or systemic problems. The lighter eye is typically regarded as the affected eye as it usually shows iris hypoplasia. It may affect an iris completely or only partially.
• Congenital Horner's syndrome - Sometimes inherited, although usually acquired
• Waardenburg's syndrome [9] - a syndrome in the which presents as a bilateral Heterochromia iris hypochromia in some cases. A Japanese review of 11 albino children with the disorder found That Had all sectoral / partial Heterochromia.
• Piebaldism - similar to Waardenburg's syndrome, a rare disorder of melanocyte development characterized by a white forelock and multiple symmetrical hypopigmented or depigmented macules.
• Hirschsprung's disease - a bowel disorder associated with Heterochromia in the form of a sector hypochromia. The affected sectors have been shown to have reduced numbers of melanocytes and Decreased stromal pigmentation.
• Incontinentia pigmenti
• Parry-Romberg syndrome

Acquired Heterochromia
Heterochromia That is acquired is usually due to injury, inflammation, the use of Certain eyedrops, or tumors.
Abnormal iris darker
• Deposition of material
o Siderosis - iron deposition within ocular tissues due to a penetrating injury and a retained iron-containing, intraocular foreign body.
o Hemosiderosis - long standing hyphema (blood in the anterior chamber) following blunt trauma to the eye may lead to iron deposition from blood products
• Use of Certain eyedrops - prostaglandin analogues (latanoprost, isopropyl unoprostone, travoprost, and bimatoprost) are used topically to lower intraocular pressure in glaucoma Patients. A concentric Heterochromia has developed in some Patients applying these drugs. The stroma around the iris sphincter muscle Becomes Darker Than the peripheral stroma. A stimulation of melanin synthesis within iris melanocytes has been postulated.
• neoplasm - melanomatous nevi and tumors.
• Iridocorneal endothelium syndrome
• Iris ectropion syndrome
Abnormal iris lighter
• heterochromic Fuchs iridocyclitis - a condition characterized by a low grade, asymptomatic uveitis in the which the iris in the affected eye Becomes hypochromic and has a washed-out, somewhat moth Eaten appearance. The Heterochromia can be very subtle, ESPECIALLY in Patients with lighter colored irides. Often it is most easily seen in daylight. The prevalence of Heterochromia associated with Fuch's has been estimated in Various studies with results suggesting That there is more difficulty recognizing iris color changes in dark-eyed individuals.
• Acquired Horner's syndrome - usually acquired, as in neuroblastoma, although Sometimes inherited.
• neoplasm - melanomas can also be very lightly pigmented, and a lighter colored iris may be a Rare Manifestation of metastatic disease to the eye.
Heterochromia has also been observed in Those with Duane syndrome.
• Chronic iritis
• Juvenile xanthogranuloma
• Leukemia and lymphoma
Central Hieterochromia

Central Heterochromia is an eye condition where there are two colors in the same iris; the central (pupillary) zone of the iris is a different color than the mid-peripheral (ciliary) zone.
Eye color is determined primarily by the concentration and distribution of melanin within the iris tissues; anything affecting Those factors may result in a difference of color being observed.
The human iris can be seen in a number of Various colors. There are three true colors in human eyes That determine the outward appearance: brown, yellow, and gray. The amount of each color an individual has determines the appearance of his or her eye color.
Eyes are displaying central Heterochromia Often Referred to as "cat eyes" Because of the appearance of a multi-colored iris. Central Heterochromia Appears to be prevalent in irises containing low amounts of melanin. Central Heterochromia does not label an eye as hazel. Because this is the outer ring of the eye is affected by central Heterochromia iris That's true color. A famous case of a person with central Heterochromia was Baroness von Rozsika Edle Wertheimstein, Whose daughter wrote: "She was a very beautiful woman ... She Had dark, dark brown eyes, but each eye had a purple ring to it, about a quarter of an inch of purple around these dark brown eyes.

Resource: http://www.answers.com/topic/heterochromia

Treatment and Therapy Hodgkin's Lymphoma

Therapy can be viewed from several aspects:
a. have or have not been treated.
b. Early stage (st I + II) or advanced stage (III + IV st)
c. Will use the means-single-therapy (radiotherapy or chemotherapy only) or a means of combination therapy (combination therapy rather than a means of combination chemotherapy).
Chemotherapy for this disease can be a single chemotherapy (using one drug), combination chemotherapy (using more drugs) and the recently developed high-dose chemotherapy plus autologous stem cell transplantation to rescue (rescue) system blood aplasia caused by high-dose chemotherapy earlier. (KDT + rPSC autologous).

I. The cases have not been previously treated (initial therapy)
a. Radiotherapy only.
In historical, just use radiotherapy, can be curative for early Hodgkin's disease (st I + II) A. but decreases when no disease below the diaphragm, therefore, stage IA and IIA are planned to be given a curative course of radiation therapy is staging laparotomy necessary to ensure the presence or absence of lesions below the diaphragm. If there is a lesion under the diaphragm, then the only use of radiotherapy is not enough, so need to be supplemented by chemotherapy. If there are signs of poor prognosis such as: B symptoms and bulky tumors, it should be a combination of radiotherapy + chemotherapy (combinations of treatment means = combined modality therapy) due to radiotherapy alone is no longer curative. To chemotherapy is usually
MOPP 6x considered sufficient as an adjuvant (additional) in radiotherapy. When no lesions below the diaphragm (evidenced by the staging-laparotomy) for stage IA are given extended field radiotherapy, for stage IIA given total nodal irradiation (TNI), is considered sufficiently curative.
b. The combination of chemotherapy + radiotherapy.
For all circumstances where there is disease below the diaphragm radiotherapy should be combined with adjuvant chemotherapy, has considered curative. Therapy with a combination of these modalities are also indicated if the disease stage IIA but the patient refused laparotomy or laparotomy is not going to do because there are contraindications.
For an advanced stage (st III and IV) the main curative treatment is chemotherapy. If there is a large lesions (bulky mass) with the addition of the letter X on a staged, it was added in place of curative doses of adjuvant radiotherapy after chemotherapy.
The combination of chemotherapy + radio is also recommended to those who show signs of poor prognosis, namely:
1. Large mediastinal mass.
 2. B-symtoms.
 3. dihilus lung abnormalities.
 4. histologinya not Lymphocytic predominant.
5. ≥ Stage III.
c. Chemotherapy
Originally given chemotherapy as primary therapy for stage III and IV, but often relapse, especially when there are bulky mass because it is for places where bulky lesions after radiotherapy adjuvant chemotherapy need to place a bulky mass was originally there. In this way the cure rate is quite high. Many experts of Medical Oncology giving chemotherapy as primary therapy since stage II coupled with adjuvant radiotherapy to the bulky mass, thus staging laparotomy needs fewer, not even necessary anymore because of this action is too invasive, while the result is the same, but there is still disagreement, especially between expert
radiotherapy with a medical oncologist.
Many chemotherapy regimens are made for Hodgkin's disease. Some are using alkylating agents, there is not. Alkylating agent is suspected as the cause of secondary cancers and sterility. Adrianisin cause cardiac abnormalities; bleomycin pulmonary abnormalities, especially when
combined with radiotherapy of the mediastinum.
Curative regimen, the regimen was always using a combination of drugs. Regimens using alkylating agents, for example:
MOPP: nitrogen mustard-M = 6mg/sqm i.v. day to 1.8
- O = Onkovin = vincristine 1.2 mg / sqm i.v. day to 1.8
- P = procarbazine 100 mg / sqm p.o 1-14 days
- P = Prednisone 40 mg / sqm p.o. repeated 1-14 days to lapse 28 days if eligible.
MOPP regimen modification was also there that Copp and LOPP.
In Copp M is replaced with C + Cyclophosphamide 800 mg / sqm iv
day to 1.8 or 3x50 mg / sqm p.o. dd day to 1-14. whereas in LOPP M replaced by L + Leukeren = chlorambucil 8 mg / sm ss po ke1-14 days.
Regimens without alkylating agent such as ABVD or ABV only.
A = adriamycin 25 mg / sqm i.v. days 1 and 14
B = bleomycin 10 mg / sqm i.v. days 1 and 14
V = vinblastine 6 mg / sqm i.v. days 1 and 14
(D) = DTIC 150 mg / sqm i.v. days 1-5 repeated intervals of 4 weeks
So the two regimens were used as initial therapy. Both regimens were not cross-resistant. Consistent with the hypothesis of Goldie and Coldman MOPP can be used first, or ABV (D) first, or alternating MOPP-ABVD-regimen MOPPABVD dst or hybrid MOPP-ABV (D), the results are equally good, but there is still disagreement.

II. Therapy cases that had been treated previously
Here therapies intended to cases of relapse, refractory since initial therapy, or after being treated several times. Sometimes MOPP or ABVD can still be used to obtain remission for two non-crossresistant this regimen, but the number of small and fast remisinya relapse. If the two standard regimens were no longer able to help other regimens used regimen-which fall in salvage-therapy (= salvage therapy). So Salvage chemotherapy is given to those who:
1. relapse after complete remission
2. resistant to therapy
Table several regimens for salvage therapy (second-line therapy in Hodgkin's Lymphoma Relapse or Resistant)
V = vinblastine 6 mg / sqm i.v. every 3 weeks
A = Adrianmisin 40 mg / sqm i.v. every 3 weeks
B = bleomycin 15 U 1-v-once every week
C = Lomustin (CCNU) 80 mg / sqm p.o. every 6 weeks
D = Dakarbasin 800 mg / sqm i-v-every 3 weeks

C = Lomustin (CCNU) 80 mg / sqm p.o. days to 1
E = etoposide 100 mg / sqm p.o. days to 1
P = Prednimustin 60 mg / sqm ivhari to 1, given the lapse 3-6minggu

E = etoposide 200 mg / sqm p.o. 1-5 days
V = vincristine 2 mg / sqm i.v. days to 1
A = adriamycin 20 mg / sqm i.v. days 1, 3-week intervals were given
M = Methyl-GAG 500 mg / sqm i.v. 1-14 days
I = ifosfamide 1 g / sqm i.v. 1-5 days
M = Methotrexate 30 mg / sqm i.v. day 3
E = etoposide 100 mg / sqm i.v. days 1-4, given the 3-week interval
C = Lomustin 100 mg / sqm p.o. days to 1
E = etoposide 100 mg / sqm h. to 1-3 and 21-23
M = Methotrexate 30 mg / sqm p.o. days 1,8,21,28, given the lapse of 6 weeks
M = Methotrexate 30 mg / sqm i.v. every 6 hours for 4 days starting the 1st day and 8 with rescue
C = Cyclophosphamide 750 mg / sqm i.v.h. to 15
H = Doxorubicin 50 mg / sqm i.v.h to 15
O = vincristine 1 mg / sqm i.v. day 15 and 22
P = Prednisone 100 mg / sqm p.o. 22-26 days, given the lapse of 4 weeks
E = etoposide 120 mg / sqm i.v. day 1,8,15
V = vinblastine 4 mg / sqm i.v. day 1,8,15
A = Ara-C 30 mg / sqm i.v. day 1,8,15
P = Platinum 40 mg / sqm i.v. days 1,8,15, repeated intervals of 4 weeks
M = Methotrexate 120 mg / sqm i.v. day 15 and 22 plus rescue
O = vincristine 2 mg i.v.h. 15 and 22
P = Prednisone 60 mg / sqm p.o. 1-14 days
L = Leukovorin rescue
A = Ara-C 300 mg / sqm i.v. day 15 and 22
C = Cyclophosphamide 750 mg / sqm i.v. days to 1
Salvage-therapy regimen regimens include: VABCD, ABDIC, CBVD, CEP, EVA, LVB, MIME, M-CHOP, CEM, EVAP, MOPLACE dll.Kemajuan field of bone marrow transplant or stem cell (stemcell) - Autologous also impact in therapy-resistant lymphoma.
In this condition given very high doses of chemotherapy to arise aplasi marrow (myeloablative chemotherapy), then performed the rescue with autologous stem cell transplant from peripheral blood taken after the previously given Hemopoetic Growth Factors.
Populations that require very high-dose chemotherapy plus stem-cell rescue (KDTrPSC) is an advanced Hodgkin's disease accompanied with poor prognosis factors which include:
1. Those who fail to obtain complete remission (CR) or partial (PR) is good (stable) (defined as very likely because of residual fibrosis with initial therapy).
2. Those who experienced progressive disease (PD) as initial therapy.
3. CR duration of less than 1 year
4. Recurrent relapses (≥ 2x) without looking at the length of remission
5. Presence of B symptoms at first relapse
6. Relapses after previously having stage IV
The factors mentioned above is also a predictor of poor outcome with treatment to the second line (salvage therapy), they are good candidates for KDTrPSC mentioned above. Those without the facto-bad factor when relapses can still be tested with a second-line chemotherapy to obtain a second CR, but likely only 35% only, the rest eventually also require KDTrPSC; even have begun to study the use of KDTrPSC as initial therapy, but there is still no conclusion .

Friday, 23 September 2011

How to Diagnose of Hodgkin's Lymphoma

Mbah Dukun Bagong the modern shaman from Medical and Health Information, explain how to diagnose Hodgkin's Lymphoma. how many ways to diagnose this disease?


1. CLINICAL (anamnesis)
Most patient complaints are enlarged lymph nodes in the neck, axilla or groin, weight loss decreases and sometimes accompanied by fever, sweating and itching

Palpation of enlarged lymph nodes in the neck especially supraclavicular, axillary and inguinal. Maybe palpable enlarged spleen and liver. Examination ENT (ear, nose, throat) needs to be done to determine the possibility of ring waldeyer involved. If this area looks to be examined because of gastrointestinal often seen together.
Routine blood tests, liver function tests and kidney function tests are an important part in medical examinations, but did not provide information about the extent of disease. or specific organ involvement. In patients with Hodgkin's disease as well as in neoplastic disease or other chronic normochromic normocytic anemia may be found in the degree is related to decreased levels of iron and iron bind capacity, but with normal iron stores or increased in the bone marrow leukomoid frequent moderate to severe reactions, especially in patients with symptoms and usually disappear with treatment.
Absolute mild peripheral eosinophilia is not uncommon, especially in patients suffering from pruritus. Also found monositosis absolute limfositopenia absoluit (<1000 cells per cubic millimeter) usually occurs in patients with advanced-stage disease. Has done an evaluation of many examinations as an indicator of disease severity.
Until now, the erythrocyte sedimentation rate is still the best monitors, but the examination is not specific and can return to normal although there are still residual disease. Another test is abnormal elevated levels of copper, calcium, lactic acid, alkaline phosphatase, lysozyme, globulin, C-reactive protein and other acute phase reactants in serum.
Fine Needle Aspiration Biopsy (FNAB) is often used in preliminary diagnosis of lymphadenopathy to identify the causes of disorders such as reaction hyperplastic lymph nodes, metastatic carcinoma and lymphoma malignum.
Another complicating aspiration biopsy cytology in the diagnosis of Hodgkin's Lymphoma or Non-Hodgkin's lymphoma is the presence of false negative aspiration biopsy is recommended to do multiple holes in some places the surface of the tumor. If found negative and cytology is also not in accordance with the clinical picture, then the best option is the incision or excision biopsy.

5. Histopathology
Biopsy of the tumor is very important, in addition to histopathological subtype diagnosis also identified although clear aspiration biopsy cytology Hodgkin's Lymphoma or Non-Hodgkin's Lymphoma. Biopsy was done not just take the network, but must be considered whether the tissue biopsy can provide adequate information. Biopsies are usually selected on the chain nodes in the neck. Lymph nodes in the groin, back of neck and submandibular not selected due to inflammatory processes, it is recommended that biopsy done under general anesthesia to prevent the influence of local injections of liquid drug which can disrupt the network architecture for a network

6. Radiology
These include:
1.    chest X-ray to determine the involvement of mediastinal lymph nodes
2.    Limfangiografi to determine the involvement of iliac lymph nodes and post-aortal area
3.USG widely used to see an enlarged lymph nodes in paraaortal and simultaneously guided fine needle aspiration biopsy for cytologic confirmation.
4. CT-scans are often used for diagnosis and evaluation of growth Hodgkin's Lymphoma

Abdominal laparotomy is often performed to see the condition lympha nodule in the para-aortic and iliac mesentery with the aim of determining the stage. Thanks to technological advances such as ultrasound radiology and CT scan plus a fine needle aspiration biopsy cytology, action laparotomy can be avoided or at least minimized.

Thursday, 22 September 2011


Today, Mbah Dukun Bagong, Indonesian Modern Shaman from Medical and Health Information, posts about malignancy of Lymphatic system, follow up of non-hodgkin lymphoma. Lets we learn Hodgkin's Lymphoma together.

1. Definition
2. Classifications
3. Etiology
4. Clinical Manfestations
5. Stages/Stadiums
6. How to Diagnose
7. Treatment and Therapy

Hodgkin's lymphoma is a limphareticular system malignancy and its supporting tissues that often attacks the lymph nodes and accompanied by the typical histopathological picture. Histopathologic characteristics are considered typical is the presence of Reed cells - Steinberg or its variants are called Hodgkin cells and pleimorfik lymph nodes picture.

 Classification of Hodgkin's lymphoma
Hodgkin's lymphoma classification.
 •  Lymphocyte-predominant (LP)
 •  Mixed cellularity (MC)
 •  lymphocyte-depletion (LD)
 • -nodular sclerosis (NS)

Parameters subtype identity more in quantity datia Reed-Steinberg cells, lymphocytes and connective tissue reaction

Lymphocyte predominant type

1.      Lymphocyte predominant type
In this type, the lymph nodes primarily composed of mature lymphocytes, some Reed-Sternberg cells. Usually found in children and the prognosis is good.

Mixed cellularity Type
2.      Mixed cellularity Type
Having pleimorfik pathological picture with plasma cells, eosinophils,
neutrophils, lymphocytes and many Reed-Sternberg cells obtained. and is extensive disease and the extranodule organ. Often accompanied by systemic symptoms such as fever, weight loss and sweating. prognosis is more worse.

lymphocyte Depleted
3.       type of lymphocyte Depleted
Similar pathological picture are diffuse histiocytic lymphoma, Reed-Sternberg cells much once and there are few other types of cells. Normally in the elderly and tend to is an extensive process (aggressive) with systemic symptoms. Poor prognosis.

Nodular Sclerosis Type
4.      Nodular Sclerosis Type
Gland contains nodules that are separated by collagen fibers. Often Reed-Sternberg cells was reported that atifik called Hodgkin cells. Often obtained in young women / teens. Mediastinal glands are often attacked.

Much progress has been achieved in the field biology of this disease. Although there are still many that have not been established. As in other malignancies, the cause of Hodgkin's disease is multifactorial and not yet completely clear.
Genetic changes, dysregulation of growth factor genes, viral and immunological effects, can all tumourigenic factor for this disease.
About the origin of Reed-Sternberg cells datia there is still disagreement as to the present. Contaminated or aggressive non-Hodgkin's lymphoma Hodgkin's probably something to do with family. When one family member suffering from Hodgkin's lymphoma, the risk of contracting other members of the tumor is larger than with anyone else that does not include the family. In people live in groups the incidence of Hodgkin's lymphoma more likely.

CLINICAL FEATURES (symptomatology)
Hodgkin's disease usually occurs as a local disease and then spread to lymphoid structures nearby and eventually expanded into non-lymphoid tissues with the possible death of the patient. Hodgkin's disease patients generally come with a mass or group of lymph nodes are solid, easily moved and are usually non-tender. Approximately half of patients present with adenopathy in the neck or supraclavicular area and more than 70 percent of patients present with superficial lymph node enlargement. Because generally painless, so the detection by the patient may be delayed until the lymph nodes is large enough.
About 60 percent of patients present with mediastinal adenopathy. It is sometimes first detected on examination of routine chest x-ray. Affected lymph nodes in Hodgkin's disease tends to centripetal or axial and different to those affected in non-Hodgkin's lymphoma showing the centrifugal tendencies of the lymph nodes epitroklear, rings waldeyer and abdomen.
The majority of patients with Hodgkin's disease have little or no symptoms related to disease. Common symptoms are mild fever that may be accompanied by night sweats. For most patients, night sweats may be the only complaint. Some patients may experience fever up and down with lots of night sweats (Pel-Epstein fever). Fever may persist for several weeks, followed by afebrile intervals. Fever and night sweats more often found in older patients and in patients with advanced-stage disease.
Another important early symptoms, weight loss is more than 10 percent in 6 months or less for no apparent reason. Other symptoms that are often found is a sense of weakness, malaise and fatigue quickly. Pruritus was found in about 10 percent of patients at diagnosis, symptoms are usually generalized and may be associated with skin rashes or even rarely the only symptom of the disease.
Mediastinal abnormalities, lung, pleura or pericardium may be accompanied by cough, chest pain, shortness of breath or osteoartropi hypertrophic, bone involvement may be accompanied by bone pain.
In some patients present with symptoms kadng superior vena cava obstruction as an initial symptom. Sudden spinal cord compression can be an early symptom but is usually a progressive disease with advanced complications. Headaches or visual disturbances may be found in patients with intracranial Hodgkin's disease and involvement of abdominal cause abdominal pain, intestinal disorders and even ascites

In this disease distinguished two kinds of staging:
 Clinical staging •
 Clinical staging is done only on the presence or absence of organ abnormalities.
 Pathological staging. •
Staging is also supported by histopathological abnormalities in the abnormal tissue. Pathological staging is expressed also on organ biopsy results, which are: liver, lung, bone marrow, lymph, spleen, pleura, bone, skin.
Staging adopted today are staging according to Ann Arbor that the appropriate modifications Cotswald conference.
Stage I: The disease affects one lymph node region or a lymphoid structure (eg: spleen, thymus, Waldeyer ring).
Stage II: The disease attacks the glands of two or more regions on one side of the diaphragm, the amount of which attacked the region represented by subscript numbers, eg: II2, II3, and so on.
Stage III: The disease attacks the region or lymphoid structure above and below the diaphragm.
III1: attack the gland splenikus hiler, seliakal, and portals
III2: attack the para-aortal glands, mesenterial and iliakal.
Stage IV: The disease attacks the organs of extra nodules, except those belonging to E (E: if the primary attack one extra-nodal organs).
A: if no symptoms of systemic
B: when accompanied by systemic symptoms are: fever ≥ 38 ˚ C is not clear why; 10% weight loss or night sweats or any combination of three symptoms that last for 6 months this disease.
X: if there is bulky mass (≥ 1 / 3 the width of the thorax and ≥ 10 cm for the size of the gland).
S: if the spleen (spleen) is affected.

To determine the extent of disease, staging procedures required certain
Procedures required to determine the level (stage) Hodgkin's disease
I. History and examination:
Identification of systemic symptoms
II. Radiological procedures:
 •  regular chest Photo
 •  CT scan of the chest (if the photos of abnormal chest)
 •  CT scan of abdomen and pelvis
 •  bipedal lymphography
III. Haematological procedures:
 •  complete blood counts
 •  LED
 •  bone marrow aspiration and biopsy
IV. biochemical procedures
 •  physiology liver Test
 •  Serum albumin, LDH, Ca
V. Procedures for specific things:
 •  laparotomy (diagnostic and staging)
 •  Abdominal ultrasound
 •  MRI
 •  Gallium scanning
 •  Technetium bone scan
 •  the liver and spleen scan

Monday, 19 September 2011

Non-Hodgkin Lymphoma

 11 September 2011, Hollywood actor Andy Whitfield was died at 39 years old. He played the part of Spartacus, a soldier condemned to fight as a gladiator and who ultimately leads a rebellion against the Romans (the Third Servile War). He was diagnosed with Non-Hodgkin Lymphoma by a doctor, March 2010.

Lymphoma malignum non-Hodgkin's or non-Hodgkin's lymphoma is a primary malignancy of lymphoid tissue wich solid.

Non-Hodgkin Lymphoma
Histological Classification of non-Hodgkin's Lymphoma
The first assumption is that the differentiation status of lymphocytes can be seen from the size and configuration of the core, lymphoid cells are small and round cells are considered as well-differentiated, and small lymphoid cells of irregular shape is considered as a poorly differentiated lymphocytes. The second assumption is the large lymphoid cells with vesicular nuclei and cytoplasm that usually has a lot of pale ascribed to the class of monocyte macrophages (histiocytes).

Signs of immunological non-Hodgkin's Lymphoma
B lymphocytes contain surface immunoglobulin which can be colored and shows the receptors for complement and Fc fraction of immunoglobulins. T lymphocytes have no surface immunoglobulin that can be colored, but have the ability to form bonds with red blood cells of sheep. Thus B and T lymphocytes can be known and specified amount in both peripheral blood and in suspensions of cells derived from lymphoid tissues. This approach has been proven that most of the HNL derived from B cells and that the proliferating cells are usually monoclonal.

Etiology and Pathogenesis
Cytogenic  abnormalities, such as chromosomal translocations. Lymphoma malignum undifferentiated cell subtypes (DU) is another high degree of malignancy HNL, rare in adults but is often found in children. Histological subtypes include Burkitt lymphoma, which is a B-cell lymphoma and has a characteristic chromosomal abnormality, which is translocated long arm of chromosome number 8 (8q) is usually to the long arm of chromosome 14 (14q +).
Viral infections, one of which is suspected of Epstein-Barr virus associated with Burkitt's lymphoma, a disease commonly found in Africa. Infection of HTLV-1 (Human T Lymphoytopic virus type 1).

Clinical Overview
Majority for asymptomatic patients as much as 2% of patients may experience fever, night sweats and weight loss.
Patients with indolent lymphoma can occur adenopathy over several months before diagnosis, although there is usually a persistent enlargement of lymph nodes nodules. For extranodule, the disease most often occurs in the stomach, lungs and bone, resulting in disease symptoms in the character which usually affect these organs.
By applying the criteria used by Rosenberg and Kaplan to determine the chains lymph nodes that are interconnected. Jones found that in 81% among 97 patients with HNL types of follicular and 90% among 93 patients with LNH type of diffuse, spread of disease also occurs by way of travel from one place to the adjacent. Nevertheless the relationship between regional lymph nodes and left neck region of the aorta in LNH follicular type is not as clear as what is seen in diffuse type HNL.
Burkitt Non-Hodgkin Lymphoma

Disease Stages
Staging is based on the type of pathology and level of involvement. Type of pathology (level of low, medium or high) based on the formulation of a new job. Level of involvement is determined according to the Ann Arbor classification.

a. New Form
Low level:
1. Small lymphocytic
2. Folicel cell mytosis
3. Folicel cells with characterized  mixture of large and small cell and mytosis

 Moderate level
4. Large Folicel cells
5. Small follicles mytosis, Diffuse
6. Large and small mixed cell, diffuse
7. Large cell, diffuse

High level: Type of an unfavorable
8. Large cell immunoblast
9. Lymphoblastic
10. Unsplit cell

b. Level of involvement is determined according to the Ann Arbor classification
Stage I:Involvement of one lymph node region (I) or the involvement of one organ or one place extralymphatic (IIE)

Stage II:
The involvement of two regions or more lymph nodes on the same side of the diaphragm (II) or local involvement in the organ or site extralymphatic and one or more regional lymph nodes on the same side of the diaphragm (IIE). Another recommendation: the number of nodal areas involved are indicated by subscript (subscript)

Stage III:
The involvement of regional lymph nodes in the second did the diaphragm (III), which can also be accompanied by a local involvement in the organ or site extralymphatic (IIIE) or both (IIIE + S) Stage IV:
Diffuse involvement or without enlarged lymph nodes. Reasons to classify patients into stage IV should be explained further by showing the place with the symbol.

Systemic symptoms
Each stage is subdivided into categories A and B. B for patients with certain symptoms and A for
those without such symptoms. Classification B will be given to patients with:
1. weight loss that can not be explained where the magnitude of more than 10% of body weight in 6 months prior to discharge from hospitalization
2.  fever that can not be explained by temperatures above 38  C.
3. night sweats.

Determination Criteria Stadium
Clinics (CS) when based solely on the results of physical examination and laboratory pathology (PS) when based on biopsy and laparotomy.

Treatment and Therapy
Therapy is usually done through a multidisciplinary approach. Therapies that can be done is:
1. Low malignancy Level / indolent:
In principle Symptomatic
- Chemotherapy: single or double medication (by mouth), if deemed necessary: COP (cyclophosphamide, Oncovin, and Prednisone)
- Radiotherapy: LNH highly radiosensitive.
Radiotherapy can be done for local and palliative. Radiotherapy: Low Dose Involved Field Radiotherapy TOI + course
2.Moderate malignancy Level / aggressive lymphoma
- Stage I: Chemotherapy (CHOP / CHVMP / BU) + radiotherapy, CHOP (cyclophosphamide, Hydroxydouhomycin, Oncovin, Prednisone)
- Stage II - IV: parenteral combination chemotherapy, radiotherapy plays for the purpose of palliation.
3. High malignancy Level  Lymphoblastic (NHL-lymphoblastic)
- Always be given treatments such as Acute lymphoblastic Leukemia (ALL)
- Re-evaluation of the treatment carried out on:
1. after the fourth cycle of chemotherapy
2. after the complete treatment cycle

Saturday, 17 September 2011

Treatment and Therapy of HEMANGIOMA

Most of  hemangiomas without complications received conservative therapy, both capillary hemangioma, cavernous or mixed. This is caused by lesions that most will involute spontaneously. In many cases of hemangiomas which received conservative therapy had better results than surgical therapy is both functional and cosmetic. There are two ways of treatment in a hemangioma.


Naturally hemangioma lesions enlarged in the first months, then reaches a large maximum and spontaneous regression after it occurs around the age of 12 months, the lesion continued to regress until the age of 5 years. Superficial hemangiomas or strawberry hemangioma is often not treated. If a hemangioma is allowed to disappear, the results appear normal skin.
Hemangiomas which require active therapy, such as hemangioma that grows on vital organs, such as the eyes, ears, and throat; bleeding hemangioma; an ulcerated hemangioma; hemangiomas with infection, hemangioma with rapid growth and tissue deformities.

1.    Compression Therapy:

There are two kinds of compression therapy can be used, they are continuous compression using an elastic bandage and intermittent pneumatic compression using the Wright Linear pump. Allegedly with the emphasis there will be discharge blood vessels will cause damage to endothelial cells which would cause the premature involution of hemangiomas.
2.    Corticosteroid therapy:
Criteria for treatment with corticosteroids are:
(1)    If involving one of the vital structures,
(2)    It grows quickly and destruction hold cosmetics,
(3)     In a mechanical hold one orifice obstruction,
(4)    There is a lot of bleeding with or without thrombocytopenia,
(5)    causes dekompensation cardiovascular.
Corticosteroids such as prednisone which make hemangioma regresses, ie to the form of strawberries, corpora cavernosa, and mix. The dose is 20-30 mg per day orally for 2-3 weeks and slowly lowered, the duration of treatment to 3 months. Therapy with corticosteroids in high doses will sometimes lead to regression of the lesions that grow rapidly. 
Hemangioma cavernosum which grows in the eyelid and interfere with vision are generally treated with steroid injections to reduce the size of the lesion rapidly, so that vision can be restored. Hemangioma cavernosum or mixed hemangiomas can be treated if the steroid is administered orally and direct injection in hemangioma. Peroral corticosteroid use in a long time can increase systemic infections, blood pressure, diabetes, stomach irritation, as well as stunted growth.
Sensitization of endothelial cells to catecholamines is the mechanism of intralesional corticosteroid injection. Therapy can occur even after enlargement of the lesion, it is temporary. The color change can be seen 2-3 days after injection and within 2-3 weeks of hemangiomas can be seen to shrink. The effectiveness of this type of therapy can usually be seen 2-3 weeks after therapy. But can also be seen after 2 months of therapy. Injection is not given to lesion but more deep in the tissues surrounding the lesion so that more space is available. Complications of this therapy, among others, can occur depigmentation and necrosis of fat. Injecting slowly with small doses can reduce the occurrence of  complications.
3.    Surgical treatment:
Incision surgery depends on the size and location of the hemangioma to be excised. Therefore radiological examination and other support is indispensable to accurately diagnose. The indication of surgical therapy on hemangiomas are:
(1)    There are signs that growth is too fast, for example, in a few weeks the lesion to be 3-4 times larger,
(2)    giant Hemangioma with thrombocytopenia,
(3)    There is no spontaneous regression, such diminution does not occur after 6-7 years.
Lesions located on the face, neck, hands or fast-growing vulva, may require local excision to control it. Embolization before surgery can be very useful if the hemangioma to be excised have a large size and location are difficult to reach with surgery. Embolization will shrink the size of the hemangioma and reduce the risk of bleeding during surgery.
4.    radiation therapy
Radiation treatment in recent years are now widely abandoned because:
(1)    The irradiation resulted in less well in children that bone growth is still very active,
(2)    Complications of malignancy that occurs in the long run,
(3)    Potential of fibrosis in the healthy skin that make difficult if the required action.
Although radiation is used extensively in the past to treat a hemangioma, but at present rarely used anymore because of long-term complications of radiation therapy, and the fact that most capillary hemangiomas will regress.
5.    sclerotic therapy
The therapy is administered by injecting the material sclerotic hemangioma lesions, for example by Namor rhocate 50%, 20% HCl kinin, Na-salicylate 30%, or hypertonic NaCl solution. However, this method is not preferred because of soreness and cause cicatrix.
Absolute alcohol is an ingredient that is often used in the treatment of sclerotic. This is due to the excellent ability to cause endothelial damage. Side effects that may occur on the injection of alcohol is the destruction of nerve tissue around, necrosis of skin, and toxicity of cardiovascular system.
6.    frozen therapy
Cool applications using liquid nitrogen. Considered quite effective given the type of superficial hemangiomas, but the therapy is rarely done because the reported cause cicatrix post-therapy.
7.    laser therapy
Irradiation with a laser performed using pulsed dye laser (PDL), which type of laser is considered particularly effective for this type of port-wine stain. This type of laser has advantages when compared with other types of lasers because of the effects are minimal keloid.
8.    embolization  therapeutic
Embolization is a technique to position the material is a thrombus into the lumen of blood vessels through the arterial catheter with fluoroscopy guidance. Embolization done when other therapeutic modalities can not be done or in preparation for surgery. Blockage of blood vessels may be permanent, semi permanent or temporary, depending on the type of materials used. Many of the embolization materials used, among other methacrylate spheres, balloon catheters, cyanoacrylate, silicone rubber, wool, cotton, gelatin sponge, polyvinyl alcohol sponge.
9.    interferon therapy
Interferon therapy works by inhibiting the growth of endothelial cells. Recombinant interferon alfa 2a or 2b is a second-line treatment in a hemangioma is very large and dangerous. Indications of the use of interferon therapy are:
(1)    No response after treatment with corticosteroids,
(2)    a contraindication by parenterally Corticosteroid long-term therapy,
(3)    the complications by corticosteroids,
(4)    the refusal of parents to therapy with corticosteroids.
In children who previously have received corticosteroid therapy, this dosage of corticosteroids should be lowered at interferon therapy. The dose of interferon is 2-3 mU/m2, injected subcutaneously once a day. The dose of interferon should always be tailored to the child's weight to prevent the proliferation of endothelial cells. Percentage of success of this therapy is 80% and can be seen after 6-10 months of therapy. Treatment with interferon is considered very effective at sufferers who experience Kassabach-Merritt syndrome. Young children who were treated with injections of interferon will have a fever for 1-2 weeks at the start of therapy. Giving acetaminophen 1-2 hours before the therapy can reduce symptoms. This therapy can cause complications include increased transaminases serum, neutropenia and anemia are temporary. The most dangerous complication is spastic diplegia, usually improved after termination of therapy, so that in children who received interferon therapy should be monitored development and neurological function at regular intervals.
10.    Chemotherapy
Vincristine is the other second-line therapy that can be used in children who do not successfully treated with corticosteroids and is also considered effective in children who suffer Kassabach-Merritt syndrome. Vincristine given intravenously with a success rate of more than 80%. Side effects of this therapy is peripheral neuropathy, constipation and hair loss. Cyclophosphamide is rarely used in a benign vascular tumor because it has a very large effect of toxicity ..
11. Antibiotics
Antibiotics are given to the ulcerated hemangioma. Also performed in a sterile wound care.


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