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.