Professional Documents
Culture Documents
STEP 1 :
STEP 2 :
1. Pathogenesis?
2. Why can he suffering cough with phlegm?
3. Why does he have shortness of breath?
4. Why the man appearance puffy face?
5. Why the PA found thoracic radiograph define opaque mass? Find the picture
6. Why the result of PE facial anhidrosis,ptosis,miosis?
7. Why does he have fever?
8. Why he has hoarse voice?
9. Why does he decrease his apetite?
10. Why he coughing up blood?
11. Etiology ?
12. What are the risk factor?
13. Clinical manifestation?
14. Classification?
15. DD of opaque mass in lung?
16. What are the Therapy?
17. Supportive examination?
18. The complication?
19. Stage of lung malignancy?
20. Diagnosis examination to evaluate lung malignancy
21. How is the prognosis of lung malignancy
STEP 3 :
1. Pathogenesis?
Local tumor growth : presented haemoptisis,wheezing,stridor,abses,atelektasis
Invasion / obstruction on nearby structure of lung : pancoast syndrome (shoulder pain)
Growth of tumor in regional lymphnode and spread occurs to lymphatic spread until
brains,bone,adrenal.if regional tumor spread into thorax that include tracheal obstruction
dyspnea,oesophageal compression with dysphagia symptom,etc
Growth in places metastases after hematogeneus spread : ex paraneoplastic syndrome
occur as a result of peptide hormon secretion by tumor due tu immunology cross
reaction between antigen of tumor tissue and antigen of normal tissue
11. Etiology ?
idiopatik
inhalation of uranium,chromade and arcent
polution
decreasing of immunity
genetic factor
lung disease
asbestos (industrial material) expossure
Chest pain
Difficulty to swallow
Fever
Weight loss
Horner’s syndrome
14. Classification?
2 mayor categories :
1. Small cell lung cancer (SCLC) : aggressive and often occur in smokers.rapidly growing
and roughly 60 percent of patient have wide spread metastatic disease at time of
diagnosis .can be called oatcell CA shape like wheat.therapy using chemotherapy.
2. Non small cell lung cancer (NSCLC) : clinical behavior of NSCLC is more variable and
depends on histologic type but 40 percent of patient have metastatic outside of chest
at the time of diagnosis .therapy using surgery
THERAPY PROGNOSIS
RISK FACTOR
ETIOLOGY PATOGENESIS
DD CLASSIFICATION
SUPPORTIVE COMPLICATION
EXAMINATION
STEP 7
1. Pathogenesis?
Sebab-sebab keganasan tumor masih belum jelas, tetapi virus, faktor lingkungan, faktor hormonal
dan faktor genetik semuanya berkaitan dengan resiko terjadinya tumor.
Permulaan terjadinya tumor dimulai dengan adanya zat yang bersifat intiation yang merangasang
permulaan terjadinya perubahan sel. Diperlukan perangsangan yang lama dan berkesinambungan
untuk memicu timbulnya penyakit tumor.
Initiati agen biasanya bisa berupa unsur kimia, fisik atau biologis yang berkemampuan bereaksi
langsung dan merubah struktur dasar dari komponen genetik ( DNA ).
Keadaan selanjutnya diakibatkan keterpaparan yang lama ditandai dengan berkembangnya
neoplasma dengan terbentuknya tumor, hal ini berlangsung lama mingguan sampai tahunan.
Kanker paru bervariasi sesuai tipe sel daerah asal dan kecepatan pertumbuhan. Empat tipe sel
primer pada kanker paru adalah karsinoma epidermoid ( sel skuamosa ), Karsinoma sel kecil ( sel
oat ), karsinoma sel besar ( tak terdeferensiasi ) dan adenokarsinoma.
Sel skuamosa dan karsinoma sel kecil umumnya terbentuk di jalan napas utama bronkial.
Karsinoma sel besar dan adenokarsinoma umumnya tumbuh dicabang bronkus perifer dan
alveoli.
Karsinoma sel besar dan karsinoma sel oat tumbuh sangat cepat sehigga mempunyai progrosis
buruk. Sedangkan pada sel skuamosa dan adenokar. Paru merupakan organ yang elastis,
berbentuk kerucut dan letaknya di dalam rongga dada atau toraksinoma prognosis baik karena
pertumbuhan sel ini lambat.
( Zerich 150105′ weblog )
2. Why can he suffering cough with phlegm?
3. Why does he have shortness of breath?
Difficulty in breathing (also known as shortness of breath, breathlessness, or dyspnea) is caused
by various mechanisms related to different problems in the body. In one’s lifetime, one may
experience rare episodes of shortness of breath as part of high levels of activity like exhaustive
exertion, or during environmental conditions such as high altitude or very warm or cold
temperatures. Other than these extreme conditions, shortness of breath is commonly a sign of a
medical problem.
5. Why the PA found thoracic radiograph define opaque mass? Find the picture
6. Why the result of PE facial anhidrosis,ptosis,miosis?
Horner syndrome
Key points
• Horner syndrome is characterized clinically by miosis, ptosis, and anhidrosis.
• The lesion is due to disruption of the oculosympathetic pathway.
• Carotid dissection is a potentially life-threatening acute etiology.
• Pharmacologic testing with cocaine or apraclonidine can confirm the clinical diagnosis
of Horner syndrome.
• Imaging of the entire oculosympathetic axis may be indicated in the evaluation of
Horner syndrome.
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. The upper lid ptosis is usually mild and can be
voluntarily overcome if the patient utilizes the levator palpebrae and frontalis muscles
excessively as these are not innervated by the oculosympathetic nerves. One way to
check for lower lid ptosis is to ask the patient to look upward slightly. In the eye with an
oculosympathetic defect, the inferior corneal margin abuts the lower lid margin (upside
down ptosis). In the normal eye, sclera is visible between the inferior corneal limbus and
the lower lid margin. This lower lid ptosis is also known as "reverse" or "upside-down
ptosis."
Apparent enophthalmos. In the relaxed state, the combined upper and lower lid ptosis
narrows the palpebral fissure and creates the false impression of
enophthalmos (Thompson 1977;Miller 1985). Measurement with an exophthalmometer
reveals the enophthalmos to be apparent only.
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. In ambient room light conditions, the anisocoria can be clinically inapparent if the
parasympathetic pupilloconstrictor activity overshadows the unequal sympathetic
pupillodilator activity between the 2 eyes. Therefore, it is important to always check the
pupils in room light and in darkness as well as with added light.
Dilation lag. A normal pupil will dilate promptly within 5 seconds after the light is
turned off. This is chiefly due to sympathetic activation of the pupillodilator that "pulls"
the pupil open. However, a Horner pupil lacks this activity and dilates slowly, over 15 to
20 seconds, from parasympathetic inhibition "letting go" of the
pupilloconstrictor (Lowenstein and Loewenfeld 1950). Because the pupils need to be
observed simultaneously in the dark, a camera with infrared viewing greatly facilitates
the examination for dilation lag.
Clinical photographs of the pupil may be useful for documentation of dilation lag.
Using a flash Polaroid or digital camera, the decreasing anisocoria between 5 and 15
seconds in darkness can be easily recorded with static photographs. Finding a change
(decrease) in anisocoria of 0.4 mm or more between 5 and 15 seconds after a light flash
is 100% specific for Horner syndrome, but unfortunately, not all Horner patients
demonstrate this finding (Kawasaki and Kardon 2004). Drowsiness causes miosis and
obscures dilation lag, so arouse the patient before testing. The dilation lag may also only
be intermittently present, and the absence of the dilation lag does not rule out Horner
syndrome (Crippa et al 2007). In the clinically suspect patient, pharmacologic testing
must be pursued.
When a patient is suspected of having a bilateral Horner syndrome, asymmetry of
pupillary dilation and pharmacologic responsiveness can no longer be used for diagnostic
purposes. Infrared computerized pupillography has been utilized to define dilation lag as
the recovery time (in seconds) to baseline pupil size after a light flash and, thus, may be
useful in detecting bilateral Horner syndrome because the recovery time is compared
against established normative values, not the patient's contralateral pupil (Smith and
Smith 1999).
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, depending on whether the patient sweats enough to notice the
asymmetry. A clinical test for anhidrosis is the iodine starch test. Powdered starch is
applied to both sides of the patient's face and the patient is warmed under a heating lamp
for several minutes. Sweat turns the powder blue and shows areas of anhydrosis.
Hemifacial sweating may also occur (Sarikaya 2011).
Iris heterochromia. Unequal iris color is suggestive of a congenital Horner syndrome
but is not pathognomonic. The iris on the side with Horner syndrome fails to develop
normal ocular pigment during infancy and is, therefore, lighter in color (Weinstein et al
1980).
Subclinical Horner syndrome. A "subclinical" Horner syndrome (ie, prior history of
unilateral ptosis and miosis that seemingly resolved clinically) may still test positive for a
defect in the oculosympathetic pathway using the pharmacologic cocaine test. Subclinical
Horner syndrome has been reported with cervical cord lesions and carotid artery
dissection (Leira et al 1998). Slavin reported 1 such case of a Horner syndrome without
anisocoria due to underlying physiologic anisocoria (Slavin 2000).
http://www.medlink.com/medlinkcontent.asp
http://lungcancer.about.com/od/Respiratory-Symptoms/a/Hoarseness.htm
Hal tersebut dipengaruhi juga oleh proses inflamasi yang terjadi dalam tubuh pasien
tersebut, pada inflamasi di produksi TNF ( Tumor Necrosis Factor ) yaitu sitokin untuk
menghambat pertumbuhan tumor dan menghancurkan sel – sel tumor. Di lain pihak, TNF
menyebabkan anoreksia yang hebat melalui efeknya pada pusat nafsu makan di
hipotalamus. TNF menimbulkan hambatan pengosongan di lambung sehingga
menimbulkan perasaan kenyang. Di samping itu TNF menghambat kerja enzim
lipoprotein lipase, yaitu enzim yang memindahkan lemak dalam serum ke sel – sel lemak
sehingga lemak disintesis dan di simpan. Dengan adanya TNF, cadangan lemak dalam
jaringan menjadi sangat menipis sehingga penderita tampak kurus. Karena walaupun
asupan nutrisi berkurang, tumor yang berkembang biak menyebabkan terjadinya
peningkatan metabolisme.Selain itu TNF dalam jumlah besar dapat menyebabkan
gangguan metabolisme berat seperti gula darah turun sampai kadar yang tidak
memungkinkan untuk hidup. Hal ini disebabkan karena penggunaan yang berlebihan
glukosa oleh otot dan hati dan gagal untuk manggantikannya.
Badan penelitian dan pengembangan kesehatan. Survei kesehatan rumah tangga
(SKRT) tahun 1995. Departemen Kesehatan Republik Indonesia, 1995.
Arif N. Batuk darah dalam pulmonologi klinik. Bagian pulmonologi FKUI; Jakarta :1992,
179-183
11. Etiology ?
- Paparan atau inhalasi berkepanjangan suatu zat yang bersifat karsinogenik :
o Asbestos mesotelioma jinak local/ganas difus dari pleura adalah tumor langka
yang secara spesifik berkaitan dengan pajanan terhadap asbes.
o Radiasi ion pekerja tambang uranium
o Radon, arsen (mis. insektisida), kromium, nikel, polisiklik hidrokarbon, vinil klorida
- Kebiasaan merokok (aktif atau pasif)
- Polusi udara
- Genetic perubahan/mutasi beberapa gen yg berperan dalam kanker paru (Proto
oncogen, Tumor suppressor gene, Gene encoding enzyme)
- Diet rendahnya konsumsi terhadap betakarotene, selenium & vit A
KELOMPOK STADIUM
Ca tersembunyi Tx, N0, M0 Sputum mengandung
sel2 ganas tetapi tidak
dapat dibuktikan
adanya tumor primer
atau metastasis
Stadium 0 Tis, N0, M0 Ca in situ
Stadium IA T1, N0, M0 Tumor termasuk T1
tanpa adanya bukti
metastasis pd KGB
regional atau tempat yg
jauh
Stadium IB T2, N0, M0 Tumor termasuk
klasifikasi T2 dengan
bukti metastasis pd KGB
regional atau tempat yg
jauh
Stadium IIA T1, N1, M0 Tumor termasuk
klasifikasi T2 dengan
bukti hanya terdapat
metastasis ke
peribronkial ipsilateral
atau hilus kelenjar limfe
; tidak ada metastasis
ke tempat yg jauh
Stadium IIB T2, N1, M0 Tumor termasuk
T3, N0, M0 klasifikasi T2 atau T3
dengan atau tanpa
bukti metastasis ke
peribronkial ipsilateral
atau hilus kelenjar
limfe; tidak ada
metastasis ke tempat yg
jauh
Stadium IIIA T1-T3, N1, N2, M0 Tumor termasuk
klasifikasi T1,T2 atau T3
dengan atau tanpa
bukti metastasis ke
peribronkial ipsilateral
atau hilus kelenjar
limfe; tidak ada
metastasis ke tempat yg
jauh
Stadium IIIB T berapapun, N3, M0 Setiap klasifikasi tumor
T4, N berapapun, M0 dg metastasis ke hilus
kontralateral atau KGB
mediastinum atau ke
skalenus atau kel limfe
supraklavikular; atau
setiap tumor yg
diklasifikasikan sebagai
T4 dg atau tanpa
metastasis ke KGB
regional; tidak ada
metastasis ke tempat yg
jauh
Stadium IV T berapapun, N Setiap tumor dengan
berapapun, M1 metastasis jauh
Non-small cell lung cancers (NSCLC) are assigned a stage from I to IV in order of severity.
In stages II and III, the cancer is confined to the lung and, possibly, the lymph nodes.
Stage IV cancer has spread outside of the lung to other parts of the body.
Small cell lung cancers (SCLC) are staged using a two-tiered system:
Limited stage (LS) SCLC refers to cancer that is confined to its area of origin in the lung and lumph
nodes.
In extensive-stage (ES) SCLC, the cancer has spread beyond the lung to other parts of the body.
http://www.webmd.com/lung-cancer/guide/stages-of-lung-cancer