LBM 6

STEP 7

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
West
Netter. atlas of human anatomy
Pierson DJ.Disorders of the pleura, mediastinum, and diaphragm. in horrisons
principles of internal medicine, ed 12. new york:Mc-Graw Hill

2. Why he has hoarse voices ?

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 ?

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.

5. Why he get pain in the lower chest and 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 ?

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. 2011 Dec;32(4):703-40 ; Am J
Respir Cell Mol Biol. 2005 Sep;33(3):216-23

journal of Molecular and Genetic Pathogenesis of Lung Cancer: Differences

Between
Small-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 ?

9. Why when he runout of medicine he suffered from cough and shortness again ?
10. What are the DD and Diagnose from the scenario ?
DIAGNOSIS
pancoast tumor infiltration
based on clinical manifestasi

The most common initial symptom

of Pancoast tumor is shoulder pain,
which may radiate down to the arm
along the ulnar nerve distribution.
Pain occurs because of tumor infiltration
of the brachial plexus,
pleura, vertebrae, or upper three ribs
Horner syndromea cluster of
symptoms that include pupil constriction
(miosis), drooping of the
upper eyelid (ipsilateral ptosis),
and an absence of sweating over
the affected side of the face (anhidrosis)
occurs in up to half of
all patients with a Pancoast tumor.
It results from involvement of the
cervical paravertebral sympathetic
chain and the stellate ganglion.

source:
http://www.jfponline.com/fileadmin/qhi_archive/ArticlePDF/FP/022020064.pdf

Differential diagnosis

General imaging differential considerations include

pulmonary metastases

mesothelioma

primary chest wall tumours

o Ewing sarcoma

o PNET

chest wall metastases

apical pleural thickening secondary to previous pulmonary tuberculosis

In addition a number of plain film mimics should be considered, including:

vascular lesions - e.g. carotid pseudoaneurym 4

anterosuperior mediastinal masses

source:
Webb WR, Higgins CB. Thoracic imaging, pulmonary and cardiovascular radiology. Lippincott Williams
& Wilkins. (2005) ISBN:078174119X. Read it at Google Books - Find it at Amazon

Rong SH. Carotid pseudoaneurysm simulating Pancoast tumor. AJR Am J Roentgenol. 1984;142 (3):
495-6. AJR Am J Roentgenol (citation) - Pubmed citation

11. What are the etiologys from the scenario ?

ETIOLOGY
The vast majority of Pancoast tumors are lung cancersthough only 5% of lung
cancers have this presentation. Non-small cell lung cancers are the most
common etiology, and adenocarcinoma and
squamous cell carcinoma are the most frequent histologic types. Small-cell
carcinomas are less common since they usually develop centrally. Rare causes of
Pancoast syndrome include other malignant
tumors (primary or metastatic), hematologic processes, infectious processes, and
other nonmalignant
conditions.
Despite the rarity of these alternate etiologies, their possibility must be investigated
prior to the initiation of therapy in order to achieve optimal outcomes. Thus, the
clinical examination must be supplemented by imaging and histologic studies.

source:
http://www.jfponline.com/fileadmin/qhi_archive/ArticlePDF/FP/022020064.pdf

12. What are the risk factor from the scenario ?

13. What are the treatments from diagnose ?
 source:
Canadian Cancer Societys Steering Committee. Canadian Cancer Statistics 2011. Toronto: Canadian
Cancer Society. ISSN: 0835-2976.

Available at: http://www.cancer.ca/Canada wide/About%20cancer/~/media/CCS/Canada

%20wide/Files%20List/English%20files%20heading/PDF%20-%20Policy%20-%20Canadian
%20Cancer%20Statistics%20-%20English/Canadian%20Cancer%20Statistics%202011%20-
%20English.ashx Accessed: January 3, 2012.