LBM 6STEP 1 Puffy face : swealling on the face . there is udema on the face because of destroy of vascularitation Hoarse voices : changes of the voice become to rough or lost because of presure of nervus laryngeus reccurens by tumor Horners syndrom : a syndrom can decrease work of nervus sympatics cerervical from cervical 8 until thoracal 1 , the manifestation facial anhidrosis , ptosis , miosis , endoftalmopati

Ptosis : is the medical term for dropping eye lid that caused by paralisis of sympatics nervush Miosis : condition when diameter of pupil < 2 mm because of decrease of nervus sympatis Facial anhidrosis : a condition in ability to sweat normally same name with hipohidrosis its means no sweat

STEP 2

1. Why the man appreance puffy face ?2. Why he has hoarse voices ?3. Why he feel decrease appetite ?4. Explain about horner syndrom / bernard syndrom ?5. Why he get pain in the lower chest and tightness when breathing ?6. Why the patient cough with blood ?7. Why the relation between aktif smoker with the desease ?8. Why the patient perceived weight loss and fever ?9. Why when he runout of medicine he suffered from cough and shortness again ?10. What are the etiologys from the scenario ?11. What are the risk factor from the scenario ?12. What are the DD and Diagnose from the scenario ?13. What are the treatments from diagnose ?STEP 3

1. Why the man appreance puffy face ?

Puffy face caused of infation and supresion to vena cava superior that can puffy face , and another syndrom is feeling foolness in the had and headache There is mass or tumor can pressure VCS

2. Why he has hoarse voices ?

Because maybe is there a mass that can press nervus laryngeus that can infuence fonation Most often caaused by problem with vocal cord , when the vocal cord has inflamation they sweal and the mass common of horse voice is a call sinus infection which can usually got away within two weeks another the hoars voice doesnt go away a few weeks its can be cause of cancer3. Why he feel decrease appetite ?

Decrease apetite because of smoking there are toxic in extrapulmoner and spread to the eshopagus and make decrease apetite or disfagia4. Explain about horner syndrom / bernard syndrom ?

Is disorder because of nervus sympatic from cervical 8 until thoracal 1 ganglion superior can make manifestation ptosis (disorder from palpebra superior looks like myastenia gravis) Tumor usually a rising at the very end of the apex lungs if the metastasis 5. Why he get pain in the lower chest and tightness when breathing ? Because of mass in the bronchus make obstruction in bronchus and the patient fells dyspnea and the are disorder when gas difution Because from mass that will grow in the bronchials segments and a barrier of the air that enters the respiratory tract . manifestation that arises is a feeling of shortness of breath due to mass obstruction and there is local pain in the chest due to supression of the mass in the lung

6. Why the patient cough with blood ?

Because mass can metastasis respiratory tract make the vasculer rupture make a coughing with blood

7. What are the relations between aktive smoker with the desease ?

There is free radical from the cigarette there patogenesis proto onkogen will be onkogen because of radiation carsinogen spesifics in the substance of ciggarette can make malignation on the lung but there is factor inactivation supresor gen of tumor and the factors else there is polimorfic gen example the gen in code but endcoding interleukin 1 and the citokrom P450 cascape 8 will be apoptosis spark and there is XRCC1 will be molekul DNA repair and EFGR or epidermal growth factor receptor can be set proliferation cells apoptosis angiogenesis and infation tumor so the horners syndrom

8. Why the patient perceived weight loss and fever ?

He lost appetite so that can the patients has weight loss Fever = because of tumor press the sweat gland cant produce sweat

9. Why when he runout of medicine he suffered from cough and shortness again ?

Because of mass the lung full in the room potensial normally that room fil if we maximal inspiration but it there is mass in normal condition can make dyspnea

10. What are the DD and Diagnose from the scenario ?

DD : cardiac temponade Right ventrikular disfunction SVCS

SVCS : lung cancer , lymphoma , maligna , benigna

DIAGNOSE SVCS because SCCSCC ( Squamos Cell Carsinoma) = from the epidemiology > 57 years oldMetastasis in the principal bronchus go to hilus gland but the patient there is metastasis spread to VCS anhidrosis , puffy face

11. What are the etiologys from the scenario ?

Lung cancer Exposure iritation free radical Metastasis from breast cancer and testis cancer Aneurisma Fibrosis Mediastinitis tuberculosis Histoplasmosis

12. What are the risk factor from the scenario ?

Smoker Cateteritation Family history of lung cancer Radiation teraphy to the chest

13. What are the treatments from diagnose ? depend of etilogy Steroid : inflamation ( glukokortikoid , dexametason ) Diuretik : decrease preload Surgery Stent Imunotherapy Stop smoking Oxigen

1.Why the man appreance puffy face ?

Swelling of the face (face oedema) which may develop if a tumour presses on a main vein coming towards the heart from the head or a blockage of a main blood vessel (superior vena cava obstruction).

The leading symptoms of SVC syndrome are facial edema, distended veins in the neck and sometimes chest, arm edema, shortness of breath, cough, facial plethora/fullness, and less commonly wheezing, lightheadedness, headaches, and even confusion.

source:Introduction to Superior Vena Cava (SVC) Syndrome_Published October 25, 2008 By Dr WestNetter. atlas of human anatomyPierson DJ.Disorders of the pleura, mediastinum, and diaphragm. in horrisons principles of internal medicine, ed 12. new york:Mc-Graw Hill

A puffy face, neck, and eyelids, coupled with dilated veins of the neck, shoulder, thorax, and upper arm (i.e., superior vena cava syndrome) may constitute the rst clinical evidence of obstruction of the superior vena cava by a neoplasm of the lung. Although the causes of superior vena cava syndrome are many and diverse, at least 80 percent are attributable to a primary carcinoma of the lung . In the patient in whom an eoplasmhas evoked acute signs andsymptomsof increased systemic venous pressure that progresses rapidly (e.g.,to laryngeal edema), early diagnosis and prompt treatmentof the neoplasm can be lifesaving. The presence of Hornerssyndromeunilateral ptosis, miosis, and anhidrosisin apatient with a carcinoma of the lung suggests a pulmonarysulcus tumor with involvement of the ipsilateral sympatheticpathway within the thoraxFishmans Pulmonary Diseases and Disorders Fourth Edition Volumes 1 & 2, Alfred P. Fishman, MD

2.Why he has hoarse voices ?

Textbook of Pulmonary Medicine, Volume 1Oleh D. Behera

Sound is produced in the larynx by vibration of the vocal cords. Resonance occurs in the pharynx, nose and mouth; articulation uses the mouth and tongue. Coughing requires adduction of the vocal cords to be effective.Innervation of the laryngeal muscles is from the vagus nerve via its branches, the superior laryngeal and recurrent laryngeal nerves. The recurrent laryngeal nerve controls abduction and adduction of the vocal cords. This nerve has a long course, from the base of the skull to the mediastinum: on the left side it loops under the aortic arch and on the right under the subclavian artery.The vocal cords are subject to high forces and so are vulnerable to voice overuse or misuse.source: Meyer TK; The larynx for neurologists. Neurologist. 2009 Nov;15(6):313-8. About the voice; Lions Voice Clinic of the University of Minnesota

3.Why he feel decrease appetite ?

From Symptoms secondary to regional metastases can be esophageal compression causes dysphagia and decrease appetite.www.merckmanuals.com/professional/pulmonary_disorders/tumors_of_the_lungs .html

The anorexia/cachexia syndrome is a multi-factorial entity. While the association between contributing factors is not clearly understood, chronic inflammation has been identified as a core mechanism. Lipolysis, muscle protein catabolism, increases in acute-phase proteins (including C-reactive protein), and a rise in pro-inflammatory cytokines (notably IL-1 [interleukin-1], IL-6 [interleukin-6], TNF [tumor necrosis factor alpha], and LIF [leukemia inhibitory factor]) are associated with the syndrome and are similar to the processes and substances found in the metabolic response to an acute injury.Inflammatory cytokines, specifically TNF, IL-1, IL-6, as well as others, may play a causative role.Anorexia may be due to the effects of inflammatory cytokines on the hypothalamus with consequent changes in the balance of neurotransmitters stimulating or inhibiting food intake. Neuropeptide Y and Agouti Related Peptide (AGRP) are appetite-stimulating neurotransmitters; conversely the Opio-melanocortin and the Cocaine Amphetamine Related Factor (CART) neurotransmitter systems inhibit food intake.In health, leptin, which is produced in fatty tissue, inhibits appetite, while ghrelin, a hormone mainly produced in the stomach, stimulates appetite; both act through their influence on the neurotransmitter systems described above. These physiologic regulators seem overwhelmed in cachectic patients(loss weight); leptin levels are low and ghrelin levels are high, but all to no avail.source:MacDonald N, Eason AM, Mazurak, et al. Understanding and managing cancer cachexia. J Am Coll Surg. 2003;197:143-161; full text.

4.Explain about horner syndrom / bernard syndrom ?

Horner syndrome (Horners syndrome) results from an interruption of the sympathetic nerve supply to the eye and is characterized by the classic triad of miosis (ie, constricted pupil), partial ptosis, and loss of hemifacial sweating (ie, anhidrosis). The term Horner syndrome is commonly used in English-speaking countries, whereas the term Bernard-Horner syndrome is common in France.Causes of Horner syndrome include the following: Lesion of the primary neuron Brainstem stroke or tumor or syrinx of the preganglionic neuron In one study, 33% of patients with brainstem lesions demonstrated Horner syndrome[2] Trauma to the brachial plexus Tumors (eg, Pancoast) or infection of the lung apex Lesion of the postganglionic neuron Dissecting carotid aneurysm In one study, 44% (65/146) of patients with internal extracranial carotid artery dissections had painful Horner syndrome, which remained isolated in half the cases (32/65)[3] Carotid artery ischemia Migraine Middle cranial fossa neoplasm

source:Wilkins, R.H., Brody, I.A., Durham, N.C. (1968) Horners syndrome. Arch. Neurol. 19: 540-542.

Clinical manifestationsHorner syndrome is caused by a lesion of the sympathetic pathway supplying the head, eye, and neck.Ptosis. There is both upper and lower lid ptosis due to loss of sympathetic innervation to the superior and inferior tarsal muscles.Miosis. The anisocoria of a Horner syndrome is generally small, about 1.0 mm or less. The miosis (smaller pupil) results from a lack of an active pupillodilator due to an oculosympathetic defect; therefore, the anisocoria is greater in darkness than in room light. Anhidrosis. Because the sympathetic plexus accompanying the internal carotid artery innervates sweat glands only to the medial forehead (Salvesen 2001), facial anhidrosis does not occur significantly with postganglionic Horner syndrome. Among patients with central and preganglionic Horner syndrome, in which there is loss of the vasomotor sympathetic fibers to the face, the patient may or may not complain of decreased sweating on 1 side.http://www.medlink.com/medlinkcontent.asp

5.Why he get pain in the lower chest and tightness when breathing ?Because there are tumor in airway and push , make dyspnea tightness when breathing

6.Why the patient cough with blood ?

Most of the lung's blood (95%) circulates through low-pressure pulmonary arteries and ends up in the pulmonary capillary bed, where gas is exchanged. About 5% of the blood supply circulates through high-pressure bronchial arteries, which originate at the aorta and supply major airways and supporting structures. In hemoptysis, the blood generally arises from this bronchial circulation, except when pulmonary arteries are damaged by trauma, by erosion of a granulomatous or calcified lymph node or tumor, or, rarely, by pulmonary arterial catheterization or when pulmonary capillaries are affected by inflammation.

source:A Merck Manual of Patient Symptoms podcast_July 2014 by Noah Lechtzin, MD, MHS

7.What are the relations between aktive smoker with the desease ?

How smoking causes cancerSmoking causes over a quarter of all cancer deaths in the UK and nearly one in five cancer cases.

This page describes how the various poisons in cigarette smoke cause cancer by damaging our DNA, preventing DNA repair and weakening the ability to remove toxins from the body.What happens in your body?Chemicals in cigarette smoke enter our blood stream and can then affect the entire body.

This is why smoking causes so many diseases, including many types of cancer, heart disease and various lung diseases.

Smoking causes at least 14 different types of cancer, you can see a diagram on thesmoking and cancerpage.Damaging our DNAThe main way that smoking causes cancer is by damaging our DNA, including key genes that protect us against cancer. Many of the chemicals found in cigarettes have been shown to cause DNA damage, including benzene, polonium-210, benzo(a)pyrene and nitrosamines.

This is already bad news, but its made worse by other chemicals in cigarettes. For example chromium makes poisons like benzo(a)pyrene stick more strongly to DNA, increasing the chances of serious damage. And chemicals like arsenic and nickel interfere with pathways for repairing damaged DNA.This makes it even more likely that damaged cells will eventually turn cancerous.Weakening the bodys defencesAs well as less effective DNA repair, smokers cant handle toxic chemicals as well as those with healthy lungs and blood.

We all have special cleaner proteins called detoxification enzymes that mop up harmful chemicals and convert them into harmless ones. But the chemicals in smoke, such as cadmium, can overwhelm these cleaners.

Other chemicals like formaldehyde and acrolein kill cilia, the small hairs that clean toxins from your airways.

Cigarette smoke also impacts the immune system increasing cells which can encourage tumour growth in the lungs and suppressing the ones which kill cancer cells.Concentration of chemicalsMost of the harmful substances in tobacco smoke are found at low levels in a single cigarette. But smokers are exposed to large amounts overall and these chemicals can build up to high levels in our bodies.

For example, heavy smokers can be exposed to up to 150 times the background level of radioactive polonium-210.Cancer is a multi-step processIt usually takes many years, or decades, for smoking to cause cancer. Our bodies are designed to deal with a bit of damage but its hard for the body to cope with the number of harmful chemicals in tobacco smoke. Over time DNA damage builds up and makes it more and more likely that our cells will become cancerous.

The pathogenesis of lung cancer is like other cancers, beginning with carcinogen-induced initiation events, followed by a long period of promotion and progression in a multistep process. Cigarette smoke both initiates and promotes carcinogenesis. The initiation event happens early on, as evidenced by similar genetic mutations between current and former smokers (e.g. 3p deletion, p53 mutations). Smoking thus causes a field effect on the lung epithelium, providing a large population of initiated cells and increasing the chance of transformation. Continued smoke exposure allows additional mutations to accumulate due to promotion by chronic irritation and promoters in cigarette smoke (e.g. nicotine, phenol, formaldehyde). The time delay between smoking onset and cancer onset is typically long, requiring 20-25 years for cancer formation. Cancer risk decreases after smoking cessation, but existing initiated cells may progress if another carcinogen carries on the process.

source:journal of N Engl J Med 2008 Sep 25;359(13):1367-80; Clin Chest Med.2011Dec;32(4):703-40 ; Am J Respir Cell Mol Biol.2005 Sep;33(3):216-23journal of Molecular and Genetic Pathogenesis of Lung Cancer: Differences BetweenSmall-Cell and Non-Small-Cell Carcinomas_Hitoshi Kitamura, Takuya Yazawa, Koji Okudela, Hiroaki Shimoyamada and Hanako Sato

8.Why the patient perceived weight loss and fever ?From Symptoms secondary to regional metastases can be esophageal compression causes dysphagia and decrease appetite.www.merckmanuals.com/professional/pulmonary_disorders/tumors_of_the_lungs .html

Cancer occurs when normal cells undergo a transformation that causes them to grow and multiply without control. The cells form a mass or tumor that differs from the surrounding tissues from which it arises. Tumors are dangerous because they take oxygen, nutrients, and space from healthy cells and because they invade and destroy or reduce the ability of normal tissues to function.Most lung tumors are malignant. This means that they invade and destroy the healthy tissues around them and can spread throughout the body.http://www.emedicinehealth.com/lung_cancer/page11_em.htm

9.Why when he runout of medicine he suffered from cough and shortness again ?

Glucocorticoids Class Summary These agents decrease the inflammatory response to tumor invasion and edema surrounding the tumor mass. They have anti-inflammatory properties and cause profound and varied metabolic effects. In addition, these agents modify the body's immune response to diverse stimuli. View full drug information Methylprednisolone (Solu-Medrol, Depo-Medrol, Medrol) One of several steroids that may be given in ED. Decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing increased capillary permeability. View full drug information Prednisone (Deltasone, Orasone, Sterapred) Useful in treatment of inflammatory and autoimmune reactions. By reversing increased capillary permeability and suppressing polymorphonuclear neutrophil (PMN) activity, may decrease inflammation. Diuretics Class Summary These agents may decrease venous return to the heart by decreasing preload, relieving the increased pressure in the superior vena cava. View full drug information Furosemide (Lasix) Increases excretion of water by interfering with chloride-binding cotransport system, which, in turn, inhibits sodium and chloride reabsorption in ascending loop of Henle and distal renal tubule. Dose must be individualized. Depending on response, administer at increments of 20-40 mg, no sooner than 6-8 h after previous dose, until desired diuresis occurs. When treating infants, titrate with 1 mg/kg/dose increments until satisfactory effect achieved.

Because medicine only treat cough, but dont treat the cause tumor or massFarmakologi dan treat. 2010. Edisi 5. FKUI

10. What are the DD and Diagnose from the scenario ?

Differential Diagnoses Acute Respiratory Distress Syndrome Cardiac Tamponade Chronic Obstructive Pulmonary Disease Mediastinitis Pneumonia, Bacterial Pneumonia, Fungal Pneumonia, Viral Syphilis : horners syndrom Tuberculosishttp://emedicine.medscape.com/article/460865-differential

11.What are the etiologys from the scenario ?

Etiology and PhysiologySince SVCS was first described by William Hunter in 1757, the spectrum of underlying conditions associated with it has shifted from tuberculosis and syphilitic aneurysms of the ascending aorta to malignant disorders. Almost 95% of SVCS cases described in published modern series result from cancer; the most common cause is small cell bronchogenic carcinoma, followed by squamous cell carcinoma of the lung, adenocarcinoma of the lung, non-Hodgkin lymphoma, and large cell carcinoma of the lung.[3] A nonmalignant cause of SVCS in cancer patients is thrombosis that is associated with intracaval catheters or pacemaker wires.[4] A rare cause of SVCS is fibrosing mediastinitis, either idiopathic or associated with histoplasmosis.[5] Additional rare causes of SVCS include metastatic germ cell neoplasms, metastatic breast cancer, colon cancer, Kaposi sarcoma, esophageal carcinoma, fibrous mesothelioma, Behet syndrome, thymoma, substernal thyroid goiter, Hodgkin lymphoma, and sarcoidosis.[6]Knowledge of the anatomy of the SVC and its relationship to the surrounding lymph nodes is essential to understanding the development of the syndrome. The SVC is formed by the junction of the left and right brachiocephalic veins in the mid third of the mediastinum. The SVC extends caudally for 6 to 8 cm, coursing anterior to the right mainstem bronchus and terminating in the superior right atrium, and extends anteriorly to the right mainstem bronchus. The SVC is joined posteriorly by the azygos vein as it loops over the right mainstem bronchus and lies posterior to and to the right of the ascending aorta. The mediastinal parietal pleura is lateral to the SVC, creating a confined space, and the SVC is adjacent to the right paratracheal, azygous, right hilar, and subcarinal lymph node groups. The vessel itself is thin-walled, and the blood flowing therein is under low pressure. Thus, when the nodes or ascending aorta enlarge, the SVC is compressed, blood flow slows, and complete occlusion may occur.The severity of the syndrome depends on the rapidity of onset of the obstruction and its location. The more rapid the onset, the more severe the symptoms because the collateral veins do not have time to distend to accommodate an increased blood flow. If the obstruction is above the entry of the azygos vein, the syndrome is less pronounced because the azygous venous system can readily distend to accommodate the shunted blood with less venous pressure developing in the head, arms, and upper thorax. If the obstruction is below the entry of the azygos vein, more florid symptoms and signs are seen because the blood must be returned to the heart via the upper abdominal veins and the inferior vena cava, which requires higher venous pressure.[7]One study suggested that the general recruitment of venous collaterals over time may lead to remission of the syndrome, although the SVC remains obstructed.[8]http://www.cancer.gov/cancertopics/pdq/supportivecare/cardiopulmonary/HealthProfessional/page6

12.What are the risk factors from the scenario ?a. Merokok Menurut Van Houtte, merokok merupakan faktor yang berperan paling penting, yaitu 85% dari seluruh kasus ( Wilson, 2005). Rokok mengandung lebih dari 4000 bahan kimia, diantaranya telah diidentifikasi dapat menyebabkan kanker. Kejadian kanker paru pada perokok dipengaruhi oleh usia mulai merokok, jumlah batang rokok yang diisap setiap hari, lamanya kebiasaan merokok, dan lamanya berhenti merokok (Stoppler,2010). According to Van Houtte, smoking is the most important contributing factor, ie 85% of all cases (Wilson, 2005). Cigarettes contain more than 4000 chemicals, which have been identified to cause cancer. Incidence of lung cancer in smokers is influenced by age started smoking, number of cigarettes smoked per day, duration of smoking, and duration of smoking cessation (Stoppler, 2010).

b. Perokok pasif Semakin banyak orang yang tertarik dengan hubungan antara perokok pasif, atau mengisap asap rokok yang ditemukan oleh orang lain di dalam ruang tertutup, dengan risiko terjadinya kanker paru. Beberapa penelitian telah menunjukkan bahwa pada orang-orang yang tidak merokok, tetapi mengisap asap dari orang lain, risiko mendapat kanker paru meningkat dua kali (Wilson, 2005).Diduga ada 3.000 kematian akibat kanker paru tiap tahun di Amerika Serikat terjadi pada perokok pasif (Stoppler,2010). More and more people are interested in the relationship between second-hand smoke, or cigarette smoke were found by others in a confined space, with the risk of lung cancer. Several studies have shown that people who do not smoke, but smoke inhalation from others, the risk of getting lung cancer is increased two times (Wilson, 2005).Allegedly there are 3,000 deaths from lung cancer each year in the United States occur in passive smokers (Stoppler, 2010).

c. Polusi udara Kematian akibat kanker paru juga berkaitan dengan polusi udara, tetapi pengaruhnya kecil bila dibandingkan dengan merokok kretek. Kematian akibat kanker paru jumlahnya dua kali lebih banyak di daerah perkotaan dibandingkan dengan daerah pedesaan. Bukti statistik juga menyatakan bahwa penyakit ini lebih sering ditemukan pada masyarakat dengan kelas tingkat sosial ekonomi yang paling rendah dan berkurang pada mereka dengan kelas yang lebih tinggi. Hal ini, sebagian dapat dijelaskan dari kenyataan bahwa kelompok sosial ekonomi yang lebih rendah cenderung hidup lebih dekat dengan tempat pekerjaan mereka, tempat udara kemungkinan besar lebih tercemar oleh polusi. Suatu karsinogen yang ditemukan dalam udara polusi (juga ditemukan pada asap rokok) adalah 3,4 benzpiren (Wilson, 2005) . Deaths from lung cancer is also associated with air pollution, but the effect is small when compared to smoking cigarettes. Deaths from lung cancer is the number two times more in urban than rural areas. Statistical evidence also suggested that the disease is more common in people with lower socioeconomic class of the low and decreased in those with higher grade. This is, in part can be explained from the fact that socio-economic groups are less likely to live closer to where they work, where the air is most likely more contaminated by pollution. A carcinogen is found in air pollution (also found in cigarette smoke) was 3.4 benzpiren (Wilson, 2005).

d. Paparan zat karsinogen Beberapa zat karsinogen seperti asbestos, uranium, radon, arsen, kromium, nikel, polisiklik hidrokarbon, dan vinil klorida dapat menyebabkan kanker paru (Amin, 2006). Risiko kanker paru di antara pekerja yang menangani asbes kira-kira sepuluh kali lebih besar daripada masyarakat umum. Risiko kanker paru baik akibat kontak dengan asbes maupun uranium meningkat kalau orang tersebut juga merokok. Some carcinogens such as asbestos, uranium, radon, arsenic, chromium, nickel, polycyclic hydrocarbons, and vinyl chloride can cause lung cancer (Amin, 2006). The risk of lung cancer among asbestos workers who handle approximately ten times greater than the general population. Lung cancer risk either due to contact with asbestos or uranium increases if the person also smoked.

e. Diet Beberapa penelitian melaporkan bahwa rendahnya konsumsi terhadap betakarotene, selenium, dan vitamin A menyebabkan tingginya risiko terkena kanker paru (Amin, 2006). Several studies have reported that low consumption of betakarotene, selenium, and vitamin A causes high risk of lung cancer (Amin, 2006).f. Genetik Terdapat bukti bahwa anggota keluarga pasien kanker paru berisiko lebih besar terkena penyakit ini. Penelitian sitogenik dan genetik molekuler memperlihatkan bahwa mutasi pada protoonkogen dan gen-gen penekan tumor memiliki arti penting dalam timbul dan berkembangnya kanker paru. Tujuan khususnya adalah pengaktifan onkogen (termasuk juga gen-gen K-ras dan myc) dan menonaktifkan gen-gen penekan tumor (termasuk gen rb, p53, dan CDKN2) (Wilson, 2005). There is evidence that family members of lung cancer patients are at greater risk of developing the disease. Cytogenetic and molecular genetic studies showed that mutations in the protooncogene and tumor suppressor genes has significance in the rise and development of lung cancer. The specific objective is the activation of oncogenes (genes including K-ras and myc) and turn off tumor suppressor genes (including the rb gene, p53 and CDKN2) (Wilson, 2005).

13.What are the treatments from diagnose ?Surgical bypassSurgical bypass of the SVC may be a useful way to palliate symptoms in carefully selected patients with SVCS. Indications for proceeding with such procedures are not fully clear. For the most part, these are patients with advanced intrathoracic disease amenable only to palliative therapy (ie, after failure of radiation therapy and chemotherapy). Patients with benign disease appear to be the best candidates for bypass.[30, 31] StentingThe principal options for endovascular therapy today are stenting, percutaneous transluminal angioplasty (PTA), thrombolysis, or some combination thereof. In most patients with SVCS, stenting of the SVC provides rapid symptomatic relief within few days (see the images below).

Superior vena cava syndrome (case 1, continued). Palmaz P308 stent mounted on 12-mm balloon was deployed in superior vena cava after it was predilated to 8 mm. Stent was subsequently dilated to 14 mm. Superior vena cava syndrome (case 1, continued). Venogram obtained after stenting shows widely patent superior vena cava with no collateral drainage. Pressure measurements after stenting showed 1- to 2-mm residual gradient. Superior vena cava syndrome (case 1, continued). Sonogram obtained 1 year after stenting shows near-normal venous pulsatility and respiratory phasicity. Patient experienced complete resolution of symptoms. SVC stenting may provide relief of severe symptoms for patients while the histologic diagnosis of the malignancy causing the obstruction is being actively pursued.[20, 25, 31] It may also be indicated in patients in whom chemotherapy or radiation has failed.[32, 33, 34] There is growing support for recommending stenting as a first-line treatment to be performed early in the management of SVCS.[32, 33, 34] A 2008 study by Rizvi et al concluded that stenting should be considered first-line therapy for SVCS of benign origin, with open surgical reconstruction still a good option if endovascular repair fails or is unsuitable.[35] The use of endovascular therapy for SVCS of malignant origin has been discussed by del Ro Sol et al.[36] Cases of excimer laser removal of pacemaker leads followed by venoplasty and stenting have been reported.http://emedicine.medscape.com/article/460865-treatment#a1128 Medication Summary Steroids and diuretics have been the mainstays of ED management. However, superior vena cava syndrome (SVCS) rarely presents as an acute life-threatening emergency. As such, considering the diagnosis may be more important than the actual definitive care when making therapeutic decisions. Glucocorticoids Class Summary These agents decrease the inflammatory response to tumor invasion and edema surrounding the tumor mass. They have anti-inflammatory properties and cause profound and varied metabolic effects. In addition, these agents modify the body's immune response to diverse stimuli. View full drug information Methylprednisolone (Solu-Medrol, Depo-Medrol, Medrol) One of several steroids that may be given in ED. Decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing increased capillary permeability. View full drug information Prednisone (Deltasone, Orasone, Sterapred) Useful in treatment of inflammatory and autoimmune reactions. By reversing increased capillary permeability and suppressing polymorphonuclear neutrophil (PMN) activity, may decrease inflammation. Diuretics Class Summary These agents may decrease venous return to the heart by decreasing preload, relieving the increased pressure in the superior vena cava. View full drug information Furosemide (Lasix) Increases excretion of water by interfering with chloride-binding cotransport system, which, in turn, inhibits sodium and chloride reabsorption in ascending loop of Henle and distal renal tubule. Dose must be individualized. Depending on response, administer at increments of 20-40 mg, no sooner than 6-8 h after previous dose, until desired diuresis occurs. When treating infants, titrate with 1 mg/kg/dose increments until satisfactory effect achieved.