NOR-LBM 6 RESPI

8/10/2019 NOR-LBM 6 RESPI

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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 veincoming towards the heart from the head or ablockage of a main blood vessel (superior

vena cava obstruction).

The leading symptoms of SVC syndromeare 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.
http://www.cancerresearchuk.org/about-cancer/coping-with-cancer/coping-physically/breathing/causes-of-breathlessness#svcohttp://www.cancerresearchuk.org/about-cancer/coping-with-cancer/coping-physically/breathing/causes-of-breathlessness#svco


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source:

Introduction to Superior Vena Cava (SVC) Syndrome_Published October 25, 2008 ByDr

West

Netter. atlas of human anatomy

Pierson DJ.Disorders of the pleura, mediastinum, and diaphragm. in horrisons

pri nciples 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 andrecurrent 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 VoiceClinic of the University of Minnesota

3. Why he feel decrease appetite ?
http://cancergrace.org/lung/author/dr-west-2/http://cancergrace.org/lung/author/dr-west-2/http://cancergrace.org/lung/author/dr-west-2/http://cancergrace.org/lung/author/dr-west-2/http://www.lionsvoiceclinic.umn.edu/page2.htmhttp://www.lionsvoiceclinic.umn.edu/page2.htmhttp://www.lionsvoiceclinic.umn.edu/page2.htmhttp://www.lionsvoiceclinic.umn.edu/page2.htmhttp://cancergrace.org/lung/author/dr-west-2/http://cancergrace.org/lung/author/dr-west-2/


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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 metabolicresponse 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 supplyto the eye and is characterized by the classic triad of miosis (ie, constricted pupil), partialptosis,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 aneurysmIn 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
http://emedicine.medscape.com/article/1212082-overviewhttp://emedicine.medscape.com/article/1212082-overviewhttp://emedicine.medscape.com/article/1212082-overviewhttp://emedicine.medscape.com/article/284011-overviewhttp://emedicine.medscape.com/article/284011-overviewhttp://emedicine.medscape.com/article/284011-overviewhttp://emedicine.medscape.com/article/1142556-overviewhttp://emedicine.medscape.com/article/1142556-overviewhttp://emedicine.medscape.com/article/1142556-overviewhttp://emedicine.medscape.com/article/284011-overviewhttp://emedicine.medscape.com/article/1212082-overview


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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, byerosion 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, p53mutations).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.


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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 BetweenSmall-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 symptomof Pancoast tumor is shoulder pain,

which may radiate down to the armalong the ulnar nerve distribution.

Pain occurs because of tumor infiltration

of the brachial plexus,

pleura, vertebrae, or upper three ribs

Horner syndromea cluster ofsymptoms that include pupil constriction(miosis), drooping of the

upper eyelid (ipsilateral ptosis),

and an absence of sweating overthe affected side of the face (anhidrosis)

occurs in up to half ofall patients with a Pancoast tumor.It results from involvement of the

cervical paravertebral sympathetic
http://www.ncbi.nlm.nih.gov/pubmed?term=Clin%20Chest%20Med.%202011%20Dec%3B32%284%29%3A703-40.http://www.ncbi.nlm.nih.gov/pubmed?term=Clin%20Chest%20Med.%202011%20Dec%3B32%284%29%3A703-40.http://www.ncbi.nlm.nih.gov/pubmed?term=Clin%20Chest%20Med.%202011%20Dec%3B32%284%29%3A703-40.http://www.ncbi.nlm.nih.gov/pubmed/16107574http://www.ncbi.nlm.nih.gov/pubmed/16107574http://www.ncbi.nlm.nih.gov/pubmed/16107574http://www.ncbi.nlm.nih.gov/pubmed/16107574http://www.ncbi.nlm.nih.gov/pubmed/16107574http://www.ncbi.nlm.nih.gov/pubmed/16107574http://www.ncbi.nlm.nih.gov/pubmed?term=Clin%20Chest%20Med.%202011%20Dec%3B32%284%29%3A703-40.


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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 previouspulmonary tuberculosis

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

vascular lesions - e.g. carotid pseudoaneurym4

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 ?
http://www.jfponline.com/fileadmin/qhi_archive/ArticlePDF/FP/022020064.pdfhttp://www.jfponline.com/fileadmin/qhi_archive/ArticlePDF/FP/022020064.pdfhttp://radiopaedia.org/articles/pulmonary-metastaseshttp://radiopaedia.org/articles/pulmonary-metastaseshttp://radiopaedia.org/articles/mesotheliomahttp://radiopaedia.org/articles/mesotheliomahttp://radiopaedia.org/articles/missing?article%5Btitle%5D=primary-chest-wall-tumourshttp://radiopaedia.org/articles/missing?article%5Btitle%5D=primary-chest-wall-tumourshttp://radiopaedia.org/articles/ewing-sarcomahttp://radiopaedia.org/articles/ewing-sarcomahttp://radiopaedia.org/articles/peripheral-primitive-neuroectodermal-tumourhttp://radiopaedia.org/articles/peripheral-primitive-neuroectodermal-tumourhttp://radiopaedia.org/articles/pulmonary-manifestations-of-tuberculosishttp://radiopaedia.org/articles/pulmonary-manifestations-of-tuberculosishttp://radiopaedia.org/articles/pulmonary-manifestations-of-tuberculosishttp://radiopaedia.org/articles/differential-of-an-anterosuperior-mediastinal-masshttp://radiopaedia.org/articles/differential-of-an-anterosuperior-mediastinal-masshttp://books.google.com/books?vid=ISBN078174119Xhttp://books.google.com/books?vid=ISBN078174119Xhttp://books.google.com/books?vid=ISBN078174119Xhttp://www.amazon.com/gp/product/078174119X?ie=UTF8&tag=radiopaediaor-20&linkCode=as2&camp=1789&creative=9325&creativeASIN=078174119Xhttp://www.amazon.com/gp/product/078174119X?ie=UTF8&tag=radiopaediaor-20&linkCode=as2&camp=1789&creative=9325&creativeASIN=078174119Xhttp://www.amazon.com/gp/product/078174119X?ie=UTF8&tag=radiopaediaor-20&linkCode=as2&camp=1789&creative=9325&creativeASIN=078174119Xhttp://www.ajronline.org/cgi/content/citation/142/3/495http://www.ajronline.org/cgi/content/citation/142/3/495http://www.ajronline.org/cgi/content/citation/142/3/495http://www.ncbi.nlm.nih.gov/pubmed/6607632http://www.ncbi.nlm.nih.gov/pubmed/6607632http://www.ncbi.nlm.nih.gov/pubmed/6607632http://www.ncbi.nlm.nih.gov/pubmed/6607632http://www.ajronline.org/cgi/content/citation/142/3/495http://www.amazon.com/gp/product/078174119X?ie=UTF8&tag=radiopaediaor-20&linkCode=as2&camp=1789&creative=9325&creativeASIN=078174119Xhttp://books.google.com/books?vid=ISBN078174119Xhttp://radiopaedia.org/articles/differential-of-an-anterosuperior-mediastinal-masshttp://radiopaedia.org/articles/pulmonary-manifestations-of-tuberculosishttp://radiopaedia.org/articles/peripheral-primitive-neuroectodermal-tumourhttp://radiopaedia.org/articles/ewing-sarcomahttp://radiopaedia.org/articles/missing?article%5Btitle%5D=primary-chest-wall-tumourshttp://radiopaedia.org/articles/mesotheliomahttp://radiopaedia.org/articles/pulmonary-metastaseshttp://www.jfponline.com/fileadmin/qhi_archive/ArticlePDF/FP/022020064.pdf


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ETIOLOGYThe 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 andsquamous cell carcinoma are the most frequent histologic types.Small-cell carcinomas are lesscommon since they usually develop centrally.Rare causes of Pancoast syndrome include other malignanttumors (primary or metastatic),hematologic processes,infectiousprocesses,and other nonmalignant

conditions.Despite the rarity of these alternate etiologies, their possibility must be investigated prior to the initiationof 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 ?
http://www.jfponline.com/fileadmin/qhi_archive/ArticlePDF/FP/022020064.pdfhttp://www.jfponline.com/fileadmin/qhi_archive/ArticlePDF/FP/022020064.pdfhttp://www.jfponline.com/fileadmin/qhi_archive/ArticlePDF/FP/022020064.pdf


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source:

Canadian Cancer Societys Steering Committee. Canadian Cancer Statistics 2011. Toronto: Canadian

Cancer Society. ISSN: 0835-2976.

Available at: http://www.cancer.ca/Canadawide/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: January3, 2012.

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NOR-LBM 6 RESPI