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
- Horner’s 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 ?

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 first 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 eoplasm has evoked acute
 signs andsymptomsof increased systemic venous pressure that progresses
rapidly (e.g.,to laryngeal edema), early diagnosis and prompt treatment of the
neoplasm can be lifesaving. The presence of Horner’s syndrome—unilateral
ptosis, miosis, and anhidrosis—in a patient with a carcinoma of the lung
suggests a pulmonary sulcus tumor with involvement of the ipsilateral
sympathetic pathway within the thorax
Fishman
2. Why he has hoarse voices ?
In a patient with lung cancer, the recurrent laryngeal nerves are vulnerable to
injury because of either direct invasion by malignancy or injury during
surgical dissection. The left vagus nerve is at greater risk than the right
because of its course from the neck down into the left aspect of the
mediastinum and across the aortic arch before giving off the left recurrent
laryngeal nerve at the level of the inferior border of the aortic arch (Fig. 99-8).
The nerve passes around the ligamen-tumarteriosumand “recurs “ along the
left tracheoesophageal groove. If either nerve is injured, unilateral vocal cord
dysfunction results in hoarseness, an increased risk of aspiration, and marked
decrease in the effectiveness of cough and the ability to clear secretions.
Fisman

3. Why he feel decrease appetite ?

4. Explain about horner syndrom / bernard syndrom ?
neoplasms may invade the brachial or cervical sympathetic plexus to cause
severe pain in the distribution of the ulnar nerve or to produce Horner
syndrome (ipsilateral enophthalmos, ptosis, miosis, and anhidrosis).
Patologi robin

This unusual location of a carcinoma of the lung was originally described by

Pancoast in 1932 as characterized by pain along the distribution of the eighth
cervical and the first and second thoracic nerves, Horner’s syndrome, local
destruction of bone by the tumor, and atrophy of hand muscles.
Fishman

Horner syndrome (Horner’s 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. Von Passow syndrome is an association of Horner
syndrome with iris heterochromia (heterochromia iridis).[1]
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
Horner syndrome is uncommon. No age, sexual, or racial predilections are known to exist.
The prognosis and the complications to be expected depend on the underlying cause of the
syndrome, as does treatment.
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 ?

6. Why the patient cough with blood ?

7. What are the relations between aktive smoker with the desease ?

Exposure to environmental carcinogens, such as those found in tobacco smoke, induce

or facilitate the transformation from bronchoepithelial cells to the malignant
phenotype. The contribution of carcinogens on transformation is modulated by
polymorphic variations in genes that affect aspects of carcinogen metabolism. Certain
genetic polymorphisms of the P450 enzyme system, specifically CYP1A1, or
chromosome fragility are associated with the development of lung cancer. These
genetic variations occur at relatively high frequency in the population but their
contribution to an individual's lung cancer risk is generally low. However, because of
 their population frequency, the overall impact on lung cancer risk could be high. In
addition, environmental factors, as modified by inherited modulators, likely affect
specific genes by deregulating important pathways to enable the cancer phenotype.

First-degree relatives of lung cancer probands have a two- to threefold excess risk of
lung cancer and other cancers, many of which are not smoking-related. These data
suggest that specific genes and/or genetic variants may contribute to susceptibility to
lung cancer. However, very few such genes have yet been identified. Individuals with
inherited mutations in RB (patients with retinoblastoma living to adulthood) and p53
(Li-Fraumeni syndrome) genes may develop lung cancer. Three genetic loci for lung
cancer risk have been identified by genomewide association studies, including 5p15
(TERT-CLPTM1L), 15q25(CHRNA5-CHRNA-3 nicotinic acetylcholine receptor
subunits), and 6p21 (BAT3-MSH5). A rare germline mutation (T790M) involving the
epidermal growth factor receptor (EGFR) maybe be linked to lung cancer
susceptibility in never smokers. Currently, however, no molecular criteria are used to
select patients for more intense screening regimens or for specific chemopreventive
strategies.

Harisson’s Principle of Internal Medicine 18th edition

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 DD and Diagnose from the scenario ?
Beberapa DD dari bayangan abnormal foto Rontgen dada:
a. Adanya gambaran lesi inflamasi akut :
Pneumoni
Abses paru
TB paru
Tumor paru benigna
Infark paru

b. Adanya bayangan suatu massa dengan kavitas :

Neoplasma
TB paru
Abses paru
c. Adanya bayangan bulat di daerah perifer paru :
Bayangan dengan batas tegas : tumor benigna, kista hidatidosa
Bayangan dengan batas tidak tegas, dengan garis2 radierkarsinoma paru
primer
Bayangan dengan batas tidak tegas, tetapi tanpa garis2 radier : umumnya
gambaran metastasis tumor pada paru.
TB paru
Lesi dengan kalsifikasi : TB paru lama, tumor benigna.
d. Adanya efusi pleura maligna :
Karsinoma/tumor primer di pleura (jarang)
 Metastasis keganasan pada pleura, tumor primernya :
o Karsinoma bronkus (paling sering)
o Karsinoma di luar dada : mamme, pancreas, uterus, gaster, dsb.

Pulmonologi, Prof. Dr. Pasiyan R. Sp,PD, FK UNDIP

11. What are the etiologys from the scenario ?

12. What are the risk factor from the scenario ?
Faktor risiko kanker paru paru
Beberapa faktor risiko seseorang menderita adalah sebagai berikut:
1. Merokok (perokok aktif). 9 dari 10 kasus kanker paru paru disebabkan oleh rokok.
Tingkat risiko utamanya diperngaruhi oleh lamanya seseorang merokok
2. Menghirup asap rokok (perokok pasif). Perokok pasif juga merupakan faktor
risiko dengan 25% peningkatan risiko terkena kanker paru paru jika pasangannya
merokok, sementaara yang terekspos asap rokok di lingkungan kerja resikonya
meningkat 17%.
3. Usia lebih dari 40 tahun
4. Paparan asbes dan gas radon
5. Sakit yyang dialami sebelumnya (mis: TB)
6. Sejarah keluarga yang terkena kanker paru-paru
7. Polusi udara di luar ruangan

Sumber : Suroyo, Joko. Herbal Penyembuhan Gangguan Sistem Pernapasan. 2010.

Yogyakarta: B First

Risk Factors

While the large majority (80–90%) of lung cancers is caused by cigarette smoking,
several other factors have been implicated, although none to the extent of tobacco.
Cigarette smokers have a tenfold or greater increase in risk of this cancer compared to
those who have never smoked. A deep sequencing study suggested that one genetic
mutation is induced for every 15 cigarettes smoked. The risk of lung cancer is lower
among persons who quit smoking than among those who continue smoking; former
smokers have a ninefold increased risk of developing lung cancer compared to men
who have never smoked versus the twentyfold excess in those who continue to smoke.
The size of the risk reduction increases with the length of time the person has quit
smoking, although generally even long-term former smokers have higher risks of lung
cancer than those who never smoked. Cigarette smoking increases the risk of all the
major lung cancer cell types. Environmental tobacco smoke (ETS) or secondhand
smoke is also an established cause of lung cancer. The risk from ETS is less than from
active smoking, with a 20–30% increase in lung cancer observed among never
smokers married for many years to smokers, in comparison to the 2000% increase
among continuing active smokers.
While cigarette smoking is the dominant cause of lung cancer, several other risk
factors have been identified, including occupational exposures to asbestos, arsenic,
bischloromethyl ether, hexavalent chromium, mustard gas, nickel (as in certain nickel-
refining processes), and polycyclic aromatic hydrocarbons. Occupational studies also
have provided insight into possible mechanisms of lung cancer induction. For
example, the risk of lung cancer among asbestos-exposed workers is increased
primarily among those with underlying asbestosis, raising the possibility that the
scarring and inflammation produced by this fibrotic nonmalignant lung disease may in
many cases (though likely not in all) be the trigger for asbestos-induced lung cancer.
Several other occupational exposures have been associated with increased rates of
lung cancer, but the causal nature of the association is not as clear.

The risk of lung cancer appears higher among individuals with low fruit and vegetable
intake during adulthood. This observation led to hypotheses that specific nutrients, in
particular retinoids and carotenoids, might have chemopreventive effects for lung
cancer. However, randomized trials failed to validate this hypothesis. In fact, studies
found the incidence of lung cancer was increased among smokers with
supplementation. Ionizing radiation is also an established lung carcinogen, most
convincingly demonstrated from studies showing increased rates of lung cancer
among survivors of the atom bombs dropped on Hiroshima and Nagasaki and large
excesses among workers exposed to alpha irradiation from radon in underground
uranium mining. Prolonged exposure to low-level radon in homes might impart a risk
of lung cancer equal or greater than that of ETS. Prior lung diseases such as chronic
bronchitis, emphysema, and tuberculosis have been linked to increased risks of lung
cancer as well.

Smoking Cessation

Given the undeniable link between cigarette smoking and lung cancer (not even
addressing other tobacco-related illnesses), physicians must promote tobacco
abstinence. Physicians also must help their patients who smoke to stop smoking.
Smoking cessation, even well into middle age, can minimize an individual's
subsequent risk of lung cancer. Stopping tobacco use before middle age avoids more
than 90% of the lung cancer risk attributable to tobacco. However, little health benefit
is derived from just "cutting back." Importantly, smoking cessation can even be
beneficial in individuals with an established diagnosis of lung cancer, as it is
associated with improved survival, fewer side effects from therapy, and an overall
improvement in quality of life. Moreover, smoking can alter the metabolism of many
chemotherapy drugs, potentially adversely altering the toxicities and therapeutic
benefits of the agents. Consequently, it is important to promote smoking cessation
even after the diagnosis of lung cancer is established.

Physicians need to understand the essential elements of smoking cessation therapy.

The individual must want to stop smoking and must be willing to work hard to
achieve the goal of smoking abstinence. Self-help strategies alone only marginally
affect quit rates, whereas individual and combined pharmacotherapies in combination
with counseling can significantly increase rates of cessation. Therapy with an
antidepressant (e.g., bupropion) or nicotine replacement therapy (varenicline, an
nicotinic acetylcholine receptor partial agonist), are approved by the U.S. Food and
Drug Administration (FDA) as first-line treatments for nicotine dependence.
 However, both drugs have been reported to increase suicidal ideation and must be
used with caution. In a randomized trial, varenicline was more efficacious than
bupropion or placebo. Prolonged use of varenicline beyond the initial induction phase
proved useful in maintaining smoking abstinence. Clonidine and nortriptyline are
recommended as second-line treatments (Chap. 395).

Inherited Predisposition to Lung Cancer

Exposure to environmental carcinogens, such as those found in tobacco smoke, induce

or facilitate the transformation from bronchoepithelial cells to the malignant
phenotype. The contribution of carcinogens on transformation is modulated by
polymorphic variations in genes that affect aspects of carcinogen metabolism. Certain
genetic polymorphisms of the P450 enzyme system, specifically CYP1A1, or
chromosome fragility are associated with the development of lung cancer. These
genetic variations occur at relatively high frequency in the population but their
contribution to an individual's lung cancer risk is generally low. However, because of
their population frequency, the overall impact on lung cancer risk could be high. In
addition, environmental factors, as modified by inherited modulators, likely affect
specific genes by deregulating important pathways to enable the cancer phenotype.

First-degree relatives of lung cancer probands have a two- to threefold excess risk of
lung cancer and other cancers, many of which are not smoking-related. These data
suggest that specific genes and/or genetic variants may contribute to susceptibility to
lung cancer. However, very few such genes have yet been identified. Individuals with
inherited mutations in RB (patients with retinoblastoma living to adulthood) and p53
(Li-Fraumeni syndrome) genes may develop lung cancer. Three genetic loci for lung
cancer risk have been identified by genomewide association studies, including 5p15
(TERT-CLPTM1L), 15q25(CHRNA5-CHRNA-3 nicotinic acetylcholine receptor
subunits), and 6p21 (BAT3-MSH5). A rare germline mutation (T790M) involving the
epidermal growth factor receptor (EGFR) maybe be linked to lung cancer
susceptibility in never smokers. Currently, however, no molecular criteria are used to
select patients for more intense screening regimens or for specific chemopreventive
strategies.

Harisson’s Principle of Internal Medicine 18th edition

13. What are the treatments from diagnose ? depend of etilogy

Cryosurgery

Good short term cure rates have been reported for small histologically confirmed SCC
treated by cryosurgery in experienced hands. Prior biopsy is necessary to establish the
diagnosis histologically. There is great variability in the use of liquid nitrogen for cryotherapy
and significant transatlantic variations in practice. For this reason caution should be
exercised in the use of cryotherapy for SCC although it may be an appropriate technique for
selected cases in specialised centres

Cryosurgery is not appropriate for locally recurrent disease or high risk tumours.
Radiotherapy

Radiotherapy is generally contraindicated in the younger patient because the scar from
surgery is usually less noticeable than the pallor and telangiectases which develop as a late
effect in irradiated skin. In some circumstances radiotherapy will give a better cosmetic
effect, particularly where loss of tissue is likely to cause cosmetic or functional impairment.
For example, the lower eyelid, the inner canthus of the eye, the lip, the tip of the nose and in
some cases the ear. SCC can be cured by radiotherapy in more than 90% of cases.

Choice of radiotherapy modality (electrons or photons) dose and technique require

experience and the involvement of a qualified clinical oncologist.

Surgical Excision

Surgical excision is the treatment of choice for the majority of cutaneous SCC. It allows full
characterisation of the tumour and a guide to the adequacy of treatment through histological
examination of the margins of the excised tissue.

Other Treatments

Other reported treatments include: topical Imiquimod, intralesional Interferon Alpha,

intralesional 5-Fluorouracil, and photodynamic therapy.Evidence for the role of these
treatments is lacking and limited to isolated case reports (Strength of Recommendation C,
Quality of Evidence IV).

Multi-professional Guidelines for the Management of the Patient with Primary Cutaneous
Squamous Cell Carcinoma

R J Motley, P W Preston, C M Lawrence