SGD 7 LBM 6 MODUL RESPIRASI

STEP 1 :

Ptosis : palpebra cannot open

Miosis : condition when diameter of pupil is smaller less than 2 mm
Facial anhidrosis : condition where the body cannot product sweat
Horner’s syndrome : the combination of clinical manifestation ptosis,miosis,facial anhidrosis
Puffy face : swelling of the face
Opaque : white appearance in radiograph

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

2. Why can he suffering cough with phlegm?

Caused by growth of abnormal cell give a pressure to nerves cough in bronchus.
Lung tumor occur in epithel bronchus give pressure to capillary until its rupture.
Normal physiology because of iritation of mucous bronchus  Cilia heal  hypertrophy
of mucous cell  hypersecret of goblet cell  cough with phlegm

3. Why does he have shortness of breath?

There are iritation of mucous bronchus  obstruction in respyratory tract  cannot
breathing easily
Pleural effusion : fluid in pleural cavity  limiting the capacity of lung

4. Why the man appearance puffy face?

Derivat symptom secondary metastasis,give preassure to VCS  blood cannot regulate to
lower part of body  edem/puffy face
Syndrome result of invasion VCS and caused headache,congestive,swelling

5. Why the PA found thoracic radiograph define opaque mass?

Caused by Infiltrat in the lung
Opaque : mass or infiltrat
Lucent : air in lung
Find the picture!
6. Why the result of Physical Examination facial anhidrosis,ptosis,miosis?
Ptosis : tumor press the symphatic nerve  nerve become paralysis.this nerve have
relation with m.levator palpebra  the muscle cannot contraction  palpebra cannot
opened
Miosis :
Facial anhidrosis : the otonom nerves (control the sweat) was damaged  destruction of
sweat gland
Horner’s syndrom Have a relation with ganglion thoracocervical

7. Why does he have fever?

He cannot produce sweat in body  heat cannot release from body

8. Why he has hoarse voice?

Cause of the nervus laryngeus reccurens have compresed by mass

9. Why does he decrease his apetite?

 Apetite controlled by hipothalamus especially nucleus ventromedial has central of
satiety,lateral nucleus is central of starve.the body adaptation with molecul HIFA (hypoxi
inducible factor 1A)  induction of leptin  loss apetite
Related with nutrition of tumor.tumor need 5x glucose than normal body.ex :
esophageal compressiondysphagia symptom,related to decreasing apetite

10. Why he coughing up blood?

Tumor can metastasis to respiratory tract  press the vascular  vascular rupture 
coughing blood

11. Etiology ?
idiopatik
inhalation of uranium,chromade and arcent
polution
decreasing of immunity
genetic factor
lung disease
asbestos (industrial material) expossure

12. What are the risk factor?

Hard smoker more than 20 cigar per day
Pollution : lung carcinogen (asbestos,arcent,nikel,chromade,zinc,uranium,etc)
Scaring of the lung as result of Previous lung disease : undergo malignant transformation
like pulmonary TB,chronic bronchitis,etc
Genetic factor : mutation of gen, mutation of lung structure
Men are high risk factore
Passive smoker in women
Work or live in bad environment
Low consumption of beta carotene,selenium and vitamin A

13. Clinical manifestation?

Shoulder pain spread into neck and head
Cough with plegm
Anoreksia
Haemoptysis
Secondary symptom:
hoarse
VCS syndrome : edem in face,dilatation vein in neck and upper arm

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

Based on biologic similarity of treatment and prognosis classificated into 4 :

1. Bronchialveolar carcinoma : spread trans bronchial,the surface of alveolar full of
tumor and it can disturb the diffusion system
2. Squamos cell : derived from bronchial epithel and there is ceratinization process
3. Large cell : ususally rises as a large mass in peripheral
4. Adenocarcinoma : most frequently occur in non-smoker

15. DD opaque mass in lung?

16. What are the Therapy?

SCLC : chemotherapy
NSCLC : surgery
Supportive treatment : controll the diet,consumtion vitamin and mineral
Treatment symptomatic : morfin,petidine analgetic
Treatment for cancer : surgery,radiotherapy,chemotherapy,combination

17. Supportive examination?

 Sumber : Aplikasi Klinis Patofisiologi – Valentina L. Brashers
18. The complication?
 STEP 4 :

CLINICAL LUNG CANCER

MANIFESTATION

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.

 Recent infections, such as bronchitis or pneumonia, or prolonged (chronic) infections, such as

tuberculosis or chronic bronchitis. Shortness of breath may be accompanied by discolored
phlegm and/or fever.
 Asthma, chronic obstructive lung disease (COPD), and emphysema: The airways are narrowed
with increased resistance to exhaling air from the lung, resulting in air entrapment in the lung.
Shortness of breath may be accompanied by wheezing. With asthma, there is usually an allergy
history, whereas with COPD or emphysema, there is usually a smoking history.
 Lung cancer and other tumors: Shortness of breath is commonly accompanied by unintentional
appetite and weight loss. There is usually a long history of heavy smoking.
 Scarring and damage of lung tissue by toxins (such as asbestosis) or by systemic illnesses (such as
rheumatoid arthritis). There is usually a known history of these systemic illnesses or occupational
exposures.
 Clot in the lung circulation (pulmonary embolus): Breathlessness is usually sudden and associated
with rapid breathing and may be accompanied by chest pain. People with blood clots in the legs
or pelvis (deep vein thrombosis, or DVT), debilitating medical conditions, immobility, or inherited
tendency of forming clots may be prone to this condition (for more information about pulmonary
embolism, see the Cardiology Patient Page by Goldhaber and Morrisson. Pulmonary embolism
and deep vein thrombosis. Circulation. 2002;106:1436–1438).
 Diseases of the lung sac (pleura): If the pleura thickens, becomes scarred, or gets filled with fluid
or blood because of infection (pleurisy), cancer, or toxins (asbestosis), or if it becomes filled with
air (called pneumothorax) because of trauma, it will hinder expansion of the lung, resulting in
shortness of breath.
 Diseases of the diaphragm and/or chest wall: The diaphragm is the muscle that expands the lung.
It may become paralyzed after chest surgery. Obesity and spine or chest wall deformities also can
produce difficulty in breathing.
http://circ.ahajournals.org/content/108/2/e11.full
4. Why the man appearance puffy face?
Puffy Face
Swollen or puffy face may be normal if you develop it occasionally or once in a blue moon
(requiring no medical work-up) however, if you are experiencing frequent episodes of facial
puffiness, you should seek immediate medical intervention as it may be a sign of a grave
underlying pathology that must be corrected. You should also observe if your family members or
siblings had/ have a history of facial puffiness after waking up in the morning.
Symptoms of Puffy Face
Knowing associated symptoms of puffy face are helpful in diagnosing the primary etiological
event that has led to the development of puffy face. The associated symptoms of facial puffiness
respond very well to lifestyle modification and home remedies to restore the natural healthy look
on your face.
1. Mild Symptoms
Mild symptoms that are associated with puffy face includes pain, redness of entire face or localized
redness at or around eyes, nose or upper/ lower face. In addition, facial puffiness may also be
associated with hives, rashes, bumps or localized lesions. Other mild symptoms include low grade
or high grade fever, nausea and sneezing.
2. Severe Symptoms
Severe symptoms that are associated with facial puffiness warrant emergent medical attention to
prevent life threatening consequences. These symptoms include swelling of throat that may lead to
difficulty with swallowing or breathing, swelling of tongue that increases the risk of sudden death
due to angioedema and obstruction of respiratory passageways, swelling of nostrils and other vital
structures that are associated with breathing.
Causes of Puffy Face
There are a number of causes that may present as puffy face. Few popular ones are listed as under:
1. Dehydration
One of the most common causes of facial puffiness is dehydration. In situations when the total
body intake of water is low, the kidneys conserve water by increasing the absorption of water that
is stored in soft tissues. Moderate dehydration leads to puffiness of face in addition to swelling of
feet and hands. The puffiness of face due to dehydration responds very well to water intake.
2. Dietary Factor
Certain foods and nutrients significantly increase the risk of developing temporary puffy face. This
includes fatty foods or beverages that dehydrate your body like coffee and tea. In addition to
 dehydration, deficiency of vitamin C also presents with puffy face and responds to supplemental
vitamin C and water- melon juice. If you consume alcohol in moderate amounts, cutting down
intake also helps tremendously.
3. Kidney Diseases
Kidney diseases (or renal failure) may also present with puffy face but in vast majority of cases,
the swelling is more pronounced in the peri-orbital region, hands and feet. Speak to your
healthcare provider if you are also experiencing urinary symptoms that points to a renal pathology.
4. Hypothyroidism
Hormonal disorders are yet another common cause of puffy face due to alteration in the normal
metabolic pathways. In addition to puffy face, you will also have other symptoms of
hypothyroidism like weight gain, constipation, dryness of skin and changes in the rhythm of heart.
5. Cushing's Syndrome
Cushing’s syndrome is marked by high cortisol levels that alter normal vascular metabolism and
leads to a round moon-shaped puffy due to deposition of fat. It may be a result of endogenous
hyper-secretion of cortisol or exogenous intake of steroids to relieve chronic inflammatory
conditions like arthritis, asthma or other similar ailments.
6. Other Causes
Other uncommon conditions that may also present with puffy face includes obesity, insect bite,
allergic reaction to drugs or certain foods, angioedema, abscess or infection of tooth, sinuses or
associated structures of head and neck region, nephritic or nephrotic syndrome, mumps and
swelling of salivary glands (like inflammation of parotid gland).
Relieves for Puffy Face
1. Dietary Methods
Dietary modifications are helpful in relieving puffiness of face without requiring any other
intervention.
 Maintain high hydration status by increasing your water intake to at least 2 liters per day.
 Salt osmotically attracts water and aggravates the symptoms of edema. Limiting your salt intake is
extremely helpful if you have puffy face due to renal problem or hypertension.
 High alcohol intake is associated with dieresis (excretion of large amounts of water in urine).
 Eat Healthy and balanced diet that is rich in quality vitamins and minerals.
2. Regular Exercises
Perform regular physical activity since sometimes the inflammatory reactions block lymphatics
leading to puffiness of face. With regular physical therapy and simple stretching exercises you can
relieve edematous swelling of the face and other parts of the body.
3. Homemade Remedies
Home remedies are helpful in alleviating the symptoms of puffy face. You can try these remedies
for speedy recovery:
 Cold Milk. In situations when the swelling on your face is due to an abscess or sore, application of
cold milk with cotton ball is helpful in reducing the pain, swelling and inflammation by acting as a
cleansing agent. Moreover, also wash your face throughout the day with cold water (without any
soap).
 Cold Creams and Lotions. You can also store your creams and lotions in refrigerator (especially in
hot humid days) to alleviate puffiness of face.
 Cold Compress. Cold compresses are helpful if you have developed an inflammatory or painful
swelling due to trauma or underlying inflammation (abscess)
4. Sleeping Position
 Changing your sleeping position also helps a great deal. Using higher pillows usually helps in
reducing edema of face due to abnormal posture. However, caution must be maintained since high
pillows or higher head support may also lead to neck-pain, insomnia or breathing difficulties.
5. Medications
Depending upon the cause of puffy face, your healthcare provider may advise you antibiotics or
anti-viral medications to relieve the symptoms due to bacterial or viral infections. You may also
get benefitted from steroids if you have developed puffy face due to allergic reaction, anaphylaxis
or insect bite.
http://www.med-health.net/Puffy-Face.html

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.

Historical note and nomenclature

The syndrome of ptosis, miosis, and anhidrosis due to a lesion in the sympathetic
pathway to the eye is known commonly as Horner syndrome. Johann Friedrich Horner
was a talented and well-respected 19th-century Swiss ophthalmologist. In 1869, he
described a 40-year-old woman with headaches who had a right droopy eyelid, smaller
right pupil, and right facial flushing. He attributed the findings to damage of the cervical
sympathetic nerves to the eye. Although his case was not the first to report the clinical
effects of damage to the cervical sympathetic nerves, his name has become an eponym
for the triad of ptosis, miosis, and anhydrosis. Professor Horner is also remembered as
the founder of Swiss ophthalmology. Because the French physiologist Claude Bernard
described the signs of sympathetic injury in animals 17 years earlier in 1852, the
syndrome is also called Bernard-Horner syndrome in some parts of the world (Pearce
1995).

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

7. Why does he have fever?

8. Why he has hoarse voice?
Hoarseness is defined as an abnormal sound when you try to speak. This may be described as
raspy, breathy, soft, tremulous or as changes in the volume of your voice. You may also
experience pain or a strained feeling when trying to speak normally.
A hoarse voice can be caused by anything that interferes with the normal vibration of the vocal
cords, such as swelling and inflammation, polyps that get in the way of the vocal cords closing
properly or conditions that result in one or both of the vocal cords becoming paralyzed.
Hoarseness is also referred to by the medical term "dysphonia."

http://lungcancer.about.com/od/Respiratory-Symptoms/a/Hoarseness.htm

9. Why does he decrease his apetite?

TNF menguluarkan enzim lipoproteinase  lemak di jaringan menipis  tampak kurus.
Gejala malaise sering ditemukan berupa anoreksia tidak ada nafsu makan, badan makin
kurus ( berat badan turun ), sakit kepala, meriang, nyeri otot, keringat malam. Gejala
malaise ini makin lama makin berat dan terjadi hilang timbul secara teratur.

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.

10. Why he coughing up blood?

Paparan dari bahan – bahan seperti asap rokok, polutan ( karsinogenik ) dalam jangka
waktu yang lama terinhalasi ke saluran pernafasan  mengaktifkan reaksi imunitas
berupa reaksi inflamasi  bronkokonstriksi, hipervaskuler dan hipersekresi mukus 
apabila hal ini terus terjadi maka akan terjadi perubahan – perubahan seperti rusaknya
silia dan perubahan metaplasia ( perubahan bentuk epitel bronkus )  pembuluh darah
disekitarnya berdilatasi dan bila berlangsung terus menerus pembuluh darah tersebut
bisa ruptur dan rusak  darahnya bisa keluar dan bercampur dengan mukus 
mengaktifkan reseptor batuk  batuk darah

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

Buku Ajar IPD ed IV jilid II. FK UI.

12. What are the risk factor?

Faktor yang mempengaruhi:

Merokok (baik perokok aktif maupun perokok pasif)

Bahaya industry
 Asbesbanyak digunakan diindustri bangunan.
Pekerja berisiko terkena 10 kali lebih tinggi dibandingkan masayarakat umum.
Mesotelioma jinak local/ganas difus dari pleura adalah tumor langka yang
secara spesifik berkaitan dengan pajanan terhadap asbes.
 Uranium, kromat, arsen (misal: insektisida yang digunakan untuk pertanian),
besi dan oksida besi .
Polusi udara
Faktor lain : makanan & kecenderungan familial
  Perokok yang makanannya rendah vitamin A memiliki risiko yang lebih
besar untuk menjadi kanker paru.
 Anggota keluarga pasien kanker paru berisiko lebih besar terkena penyakit
ini.
Sylvia A. Price & Lorraine M. Wilson. Patofisiologi ed 6 vol 2. EGC.

13. Clinical manifestation?

Ca bronkogenik :
Batuk  gejala umum yg sering diabaikan atau dianggap sebagai akibat merokok atau
bronchitis
Hemoptisis
Gejala awal : mengi local & dispnea ringan akibat obstruksi bronkus
Nyeri dada dapat timbul dalam berbagai bentuk  perasaan sakit atau tidak enak akibat
penyebaran neoplastik ke mediastinum
Nyeri pleuritik  bila terjadi serangan sekunder pada pleura akibat penyebaran
neoplastik atau pneumonia
Pembengkakan jari yg timbul cepat  dikaitkan dg Ca bronkogenik (30% kasus NS CLC)
Gejala2 umum : anoreksia, lelah, ↓ BB
Gejala penyebaran intratorax atau extrathorax :
 Penyebaran local tumor ke struktur mediastinum  suara serak akibat terserangnya saraf
laringeus rekuren
 Disfagia  keterlibatan esophagus
 Peralisis hemidiafragma  keterlibatan saraf frenicus
 Penekanan VCS  sindrom Vena cava (pelebaran vena di leher & edem pada wajah, leher &
lengan atas)
 Nyeri dada atau temponade jantingnakibat penyebaran ke dinding dada atau pericardium
secara terpisah
 Tumor2 yg berkembang di apex paru (tumor Pancoast) dapat melibatkan plexus brachialis 
nyeri & kelemahan pada bahu dan lengan bagian yg terkena; ganglion simpatikus dapat
terkena  sindrom Horner unilateral (ptosis & kontriksi pupil unilateral serta tidak adanya
produksi keringat pada bag yg sama dg wajah)
Gejala ekstrathorax bergantung pada tempat metastasis. Struktur yg sering terserang : KGB
skalenus, kel adrenalis (50%), hati (30%), otak (20%), tulang (20%), ginjal (15%).
 Sindrom paraneoplastik : berkaitan dg kanker paru
 Sindrom endokrin (12%)
 Tumor sel oat : menghasilkan hampir seluruh hormone polipeptida, seperti hormone paratiroid
(PTH), hormone adrenokortikotropik (ACTH), atau hormone antidiuretik (ADH)gejala
hiperparatiroid, sindrom Cushing, sindrom ketidaktepatan sekresi ADH (SIADH) berhubungan dg
retensi cairan & hiponatremia.
 Sindrom jar ikat rangka : jari tabuh (biasanya pada NS CLC) timbul pada 30% kasus dan
osteoartropati hipertrofik (HOA) hingga 10% kasus (biasanya pada adenoCa)
 Gejala sistemik : anoreksia, ↓ BB, dan kakeksia pada 30% kasus adalah sindrom paraneoplastik
yg tidak diketahui asalnya.
Sylvia A. Price & Lorraine M. Wilson. Patofisiologi ed 6 vol 2. EGC.
14. Classification?
Secara patologi, untuk menentukan terapi:

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.

 Sumber : Buku Saku Patofisiologi Corwin Oleh Elizabeth J. Corwin

15. DD of opaque mass in lung?

16. What are the Therapy?
 Sumber : Aplikasi Klinis Patofisiologi – Valentina L. Brashers
17. Supportive examination?
18. The complication?
19. Stage of lung malignancy?
 System stadium TNM Internasional atau Kanker paru 1997 American Joint Committee on
Cancer (dimodifikasi dari Mountain CF : Revisions in the international system for staging lung
cancer, chest 111 : 1710-1717, 1997) :

Gambaran TNM DEFINISI

STATUS TUMOR PRIMER
T0 Tidak terbukti adanya tumor primer
Tx Ca yg tersembunyi terlihat pada
sitologi bilasan bronkus, tetapi tidak
terlihat pada radiogram atau
bronkoskopi
Tis Ca in situ (ditemukan sel tumor di
suatu tempat & belum menyebar)
T1 Tumor berdiameter ≤ 3 cm dikelilingi
paru atau pleura viseralis yg normal
T2 Tumor berdiameter > 3 cm atau ukuran
berapapun yg sudah meyerang pleura
viseralis atau mengakibatkan atelektasi
yg meluas ke hilus; harus berjarak 2cm
dari karina, tetapi tidak mengenai
karina
T3 Ukuran tumor diameter 5 cm
T4 Tumor berukuran berapapun dg
perluasan langsung pada dinding dada,
diafragma, pleura mediastinalis, atau
pericardium tanpa mengenai jantung,
pembuluh darah besar, trachea,
esophagus, atau korpus vertebra; atau
dalam jarak 2 cm dari karina , tetapi
tidak mengenai karina

KETERLIBATAN KGB REGIONAL (N)

N0 Tidak dapat terlihat metastasis pd
KGB regional
N1 Metastasis pd peribronkial dan/atau
kelenjar2 hilus ipsilateral
N2 Metastasis pd mediastinal ipsilateral
atau KGB subkarina
N3 Metastasis pd mediastinal atau KGB
hilus kontralateral; KGB skalenus
atau supraklavikular ipsilateral atau
kontralateral
METASTASIS JAUH (M)
M0 Tidak diketahui adanya metastasis
jauh
M1 Metastasis jauh terdapat pd tempat
tertentu (missal otak)

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

Sylvia A. Price & Lorraine M. Wilson. Patofisiologi ed 6 vol 2. EGC.

Non-small cell lung cancers (NSCLC) are assigned a stage from I to IV in order of severity.

 In stage I, the cancer is confined to the lung.

 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

20. Diagnosis examination to evaluate lung malignancy

 Sumber : Aplikasi Klinis Patofisiologi – Valentina L. Brashers
21. How is the prognosis of lung malignancy