LBM 6

STEP 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.
2.
3.
4.
5.

Why the man appreance puffy face ?

Why he has hoarse voices ?
Why he feel decrease appetite ?
Explain about horner syndrom / bernard syndrom ?
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 cancer
3. 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 disfagia
4. 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 SCC
SCC ( Squamos Cell Carsinoma) = from the
epidemiology > 57 years old
Metastasis in the principal bronchus go to hilus
gland but the patient there is metastasis spread to
VCS anhidrosis , puffy face
11.
-

Lung cancer
Exposure iritation free radical
Metastasis from breast cancer and testis cancer
Aneurisma
Fibrosis
Mediastinitis tuberculosis
Histoplasmosis
12.

What are the etiologys from the scenario ?

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 )

1.

Diuretik : decrease preload

Surgery
Stent
Imunotherapy
Stop smoking
Oxigen

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
West
Netter. atlas of human anatomy
Pierson 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 thorax
Fishmans Pulmonary Diseases and Disorders Fourth Edition Volumes 1 & 2, Alfred P.
Fishman, MD

2.

Why he has hoarse voices ?

Textbook of Pulmonary Medicine, Volume 1

Oleh 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/tu
mors_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 manifestations
Horner 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 cancer

Smoking 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 the smoking
and cancer page.

Damaging our DNA

The 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 defences

As 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 chemicals
Most 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 process

It 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. 2011 Dec;32(4):703-40 ; Am J Respir Cell Mol Biol. 2005 Sep;33(3):216-23

journal of Molecular and Genetic Pathogenesis of Lung Cancer: Differences
Between
Small-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/tu
mors_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.

Methylprednisolone (Solu-Medrol, Depo-Medrol, Medrol)

View full drug information

One of several steroids that may be given in ED. Decreases inflammation by suppressing migration of
polymorphonuclear leukocytes and reversing increased capillary permeability.

Prednisone (Deltasone, Orasone, Sterapred)

View full drug information

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.

Furosemide (Lasix)

View full drug information

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
mass
Farmakologi 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

Tuberculosis

http://emedicine.medscape.com/article/460865-differential

11. What are the etiologys from the scenario ?

Etiology and Physiology

Since 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/HealthP
rofessional/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 bypass

Surgical 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]
Stenting

The 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.

Methylprednisolone (Solu-Medrol, Depo-Medrol, Medrol)

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One of several steroids that may be given in ED. Decreases inflammation by suppressing migration of
polymorphonuclear leukocytes and reversing increased capillary permeability.

Prednisone (Deltasone, Orasone, Sterapred)

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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.

Furosemide (Lasix)

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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.