STEP 7

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 ?

a) Kanker paru sel kecil (small cell lung cancer, SCLC)
Gambaran histologist khas : dominasi sel2 kecil hamper semua diisi mucus
dg sebaran kromatin yg sedikit sekali tanpa nucleoli. Disebut juga “oat cell
carcinoma” karena bentuknya mirip biji gandum. Sel ini cenderung
berkumpul sekeliling pembuluh darah halus menyerupai pseudoroset. Sel2
yg bermitosis banyak sekali ditemukan begitu juga gambaran nekrosis. DNA
yg terlepas myebabkan warna gelap sekitar pembuluh darah.
b) Kanker paru sel tidak kecil (non small cell lung cancer, NSCLC)
Termasuk didalamnya adalah epidermoid, adenokarsinoma, tipe-tipe sel
besar/campuran dari ketiganya.
Karsinoma sel sqamos berciri khas proses kreatinisasi & pembentukan
“bridge” intraseluler. Secara sitologi adanya perubahan nyata dari dysplasia
squamosa ke Ca insitu.
Diagnosis terlokalisasi, diatasi dengan reseksi bedah.

Buku Ajar IPD ed IV jilid II. FK UI.

PERBEDAAN SCLC NSCLC
Histologi Sitoplasma sedikit; nucleus Sitoplasma banyak; nucleus
kecil hiperkromatik dengan pleomorfik dengan pola
pola kromatin halus; kromatin kasar; nucleolus
nucleolus tidak jelas; sering mencolok; arsitektur
lembaran2 yg difus glandular atau skuamosa
Penanda neuroendokrin Biasanya ada Biasanya tidak ada
(missal granula dense core
pada mikroskop electron;
ekspresi kromogranin,
enolase spesifik neuron,
sinaptofisin)
Penanda epitel (antigen Ada Ada
membrane epitel, antigen
karsinoembrionik, dan
filamen intermediate
sitokeratin)
Musin Tidak ada Ada pada adenokarsinoma
Pembentukan hormone Hormone adenokorteks, Parathyroid hormone-
peptide hormone antidiuretik, related peptide (PTH-rp)
peptide pelepas gastrin,
kalsitonin
Kelainan gen penekan
tumor
- Delesi 3p - >90% - >80%
- Mutasi RB - Sekitar 90% - Sekitar 20%
- Mutasi - Sekitar 10% - >50%
p16/CDKN2A
- Mutasi TP53 - >90% - >50%
Kelainan onkogen
dominan - <1% - Sekitar 30% (adeno
- Mutasi K-RAS - >50% Ca)
- Ekspresi berlebihan - >50%
family MYC
Respon terhadap Sering respon tuntas Jarang respon tuntas
kemoterapi & radioterapi
Robbins Kumar. Buku Ajar Patologi ed 7 vol 2. EGC.
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