lung ca-diagnosis & mx

PowerPoint Presentation: 

DR.RAJU Post Graduate Dept.of Pulm.medicine BRONCHOGENIC CARCINOMA Diagnosis and Treatment

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ONCOGENES AND LUNG CANCER: 

ONCOGENES AND LUNG CANCER The most prominent - Deletion of the short arm of chromosome 3. DNA losses on chromosomes like 13,17,1,7,9,13-16 and 21. DNA loss has been localized to the rb locus on chromosome 13. Point mutations in the members of ras family and changes in the c- myc , N- myc,L - myc and c- myb are seen in lung cancer.

Presenting Symptoms : 

Presenting Symptoms

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Although many smokers cough, lung cancer patients usually admit to a change in the character of their cough . The cough can increase in frequency or strength or may not be relieved with local measures.

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Chest pain can be present in 25% to 50% . The pain is generally dull in nature , tends to be persistent, remains in the same location, and is not relieved with local measures. Chest pain is usually related to involvement of the pleura but can be related to extension into the mediastinum or chest wall. Chest pain in and of itself does not preclude the patient from consideration for surgery with curative intent

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Dyspnea is frequently a complaint of patients who present with bronchogenic carcinoma, occurring in half of all new patients at presentation. reasons for dyspnea includes: - pulmonary embolism - superior vena cava syndrome - deconditioning - reactive airway disease - endobronchial obstruction with tumor - prior obstructive pneumonia - hemoptysis , hemorrhage - malignant pleural effusion - extrinsic compression of the airway by tumor

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Hemoptysis in a smoker should always raise the suspicion of lung cancer. Present as blood streaking of the sputum and can occur over a lengthy period of time before presentation.

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chest radiograph can be normal up to 5% . of those with a smoking history and a normal radiograph can harbor lung cancer. Because of the vascular nature of lung cancer, patients can also present with massive hemoptysis . In one series of patients with massive hemoptysis , 20% had an underlying diagnosis of lung cancer.

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Weight loss, a nonspecific symptom, in the right clinical setting should raise the suspicion of both lung cancer and metastatic disease. Weight loss alone has been correlated with an advanced presentation and poor outcome from lung cancer

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Hoarseness of voice in lung cancer is almost always caused by involvement of left recurrent laryngeal nerve. New onset hoarseness in a smoker should always be investigated to ruleout lung cancer. Phrenic nerve palsy may occur due to local invasion of the nerve by the tumour or by the mebiastinal lymphnodes present along their path.

PowerPoint Presentation: 

Damage to the phrenic nerve results in paralysis of that hemi diaphragm, with consequent volume loss. This may cause dyspnoea especially in lying down position. Dysphagia may occur from oesophageal obstruction by bulky medistinal adenopathy. Strido r occurs due to narrowing of tracheal lumen. Direct tracheal involvement by the tumour or rarely bilateral vocal cord paralysis can lead to stridor .

Expanded Clinical Evaluation : 

Expanded Clinical Evaluation Symptoms Elicited in History: Constitutional—weight loss greater than 10 lb Musculoskeletal—focal skeletal pain Neurologic—headaches, syncope, seizures, extremity weakness, recent change in mental status Signs Found on Physical Examination: Lymphadenopathy (>1 cm) Hoarseness, superior vena cava syndrome Bone tenderness Hepatomegaly (>13-cm span) Focal neurologic signs, papilledema Soft tissue mass Routine Laboratory Tests : Hematocrit less than 40% in males Hematocrit less than 35% in females Elevated alkaline phosphatase , GGT, AST, calcium AST, aspartate aminotransferase ; GGT, γ- glutamyl transpeptidase .

PowerPoint Presentation: 

Superior vena cava syndrome is more commonly seen in patients with smallcell lung cancer . Occurs du to compression of the SVC by the: - enlarged infiltrated paratracheal lymph node/ - direct extension of the primary mass - rarely due to intravascular thrombus formation as a part of para neoplastic manifestation. Superior vena cava syndrome

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Characterized by: - puffiness of face - congestion of face and neck - dry cough - distended non pulsatile veins in the neck and the presence of collateral veins draining from above downwards from chestwall and abdomen. - Associated hoarseness due to congestion of vocal cords.

Overview…: 

Overview…

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Early diagnosis of lung cancer Transbronchial needle aspiration [TBNA] T N M staging of lung cancer Approach to the management of lung cancer

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Surgical management of lung cancer Radiation Therapy In Lung Cancer Chemotherapy in Lung Cancer Extrapulmonary syndromes associated with lung tumors

EARLY DIAGNOSIS OF LUNG CANCER: 

EARLY DIAGNOSIS OF LUNG CANCER

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Identifying the risk groups & factors Markers for genetic predisposition Molecular markers Screening tools – sputum cytology & chest x ray sputum immuno staining DNA cytometry Flourescence bronchoscopy Spiral CT of the chest

Risk factors-High risk groups: 

Risk factors-High risk groups Smoking:Active /Passive Asbestos Insulation workers, shipyard workers Some increase in risk after 10 years. Arsenic Smelter workers, vineyard workers. More in upper lobes, may have multiple primaries. Nickel Refinery workers. Squamous cell type common.

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Radiation Uranium mining, haematite mining, hard rock mining. Majority oat cell type due to radon exposure. Chromium Chromium ore processing, pigment manufaturers . Mostly squamous cell type . Chloro methyl ethers – oat cell common Mustard gas – squamous cell and undifferentiated cell carcinomas m ore common.

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Metabolic phenotypes: -Aryl hydrocarbon hydroxylase - Debrisoquine hydoxylation -Glutathione-s- transferase activity & -DNA repair capacity possible markers of genetic susceptibility to lung cancer. Markers for genetic predisposition

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Molecular markers Changes in genes,gene products and chromosomal abnormalities are advocated as a biomarkers of pre malignancy Ras family- commonly found as abnormal in lung cancer K- ras mutations :associated with a less aggressive course of non-small cell lung cancer . Changes in H- ras : are associated with more aggressive clinical course. Her2/ neu L: is over expressed and detected in sputum of several NSLC in pre- neoplastic , metaplastic and dysplastic stages.

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Sputum immuno staining CE 407 and BL 99 – 57 are the two monoclonal antibodies which give positive immunoperoxidase reactions in patients 78 – 80% with either squamous cell or adenocarcinoma diagnosed on sputum cytology. - doesn’t bind to small cell ca- D/D Another MSAb (6421 – 112) can detect early non-small cell lung cancer much before than conventional means.

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A nuclear ribonucleoprotein — hnRNP A2/B1 —was found to be overexpressed in most lung cancer cell types as well as transformed epithelial cells. PCR-based assays can detect one mutant-containing cell among an excess of 100,000 normal cells.

DNA cytometry: 

DNA cytometry Rapid DNA cytometry can detect precancerous and non precancerous pulmonary squamous dysplasias Lead time of 6 months over conventional methods

FLUORESCENCE BRONCHOSCOPY for LOCALIZATION of EARLY LUNG CANCER: 

FLUORESCENCE BRONCHOSCOPY for LOCALIZATION of EARLY LUNG CANCER

PowerPoint Presentation: 

Blue light rather than a white light is employed for illumination Premalignant and malignant tissue is distinguished by a change in color from normal tissue without the need for fluorescence-enhancing drugs. Demonstrates detection of dysplasia, carcinoma in situ, and early invasive cancers not visible by standard white light bronchoscopy (WLB).( 271 % increased relative positivity compared to conventional)

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C onventional white-light bronchoscopy Only 30% to 40% of carcinoma in situ are visible. When the bronchial surface is illuminated by light, the light can be reflected, back-scattered, absorbed, or induce tissue fluorescence. The tissue auto fluorescence is not visible because the intensity is very low and overwhelmed by the background illuminating light.

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Auto fluorescence bronchoscopy The tissue auto fluorescence can be made visible to enhance our ability to localize areas of intraepithelial neoplasia in the tracheal bronchial tree. When the bronchial surface is illuminated by violet or blue light (400 to 440 nm) normal tissues have significantly higher fluorescence intensity compare to dysplastic lesions or carcinoma in situ, especially in the green region of the emission spectrum.

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The major portion of the fluorescence signal comes from the submucosa . A decrease in the extracellular matrix in the submucosa , such as from the secretion of cancerous tissues will result in a decrease in the amount of fluorophores or the quantum yield of these molecules. Due to the increased absorption of the blue light and the fluorescent light by blood , the fluorescence intensity of these lesions is decreased.

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A third reason for the decrease in auto fluorescence in dysplastic tissues and carcinoma in situ is the increase in thickness of the epithelial layer. This thickening impedes transmission of the blue light to the submucosa and the fluorescent light from the submucosa to the bronchial surface.

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These effects are particularly pertinent to the green region of the auto fluorescence spectra because the absorption characteristics of bronchial tissue and blood favor the absorption of green light . These differences in the autofluorescence property of normal, preneoplastic , and neoplastic tissues were used in the development of the lung imaging fluorescence endoscopy (LIFE) device for the detection and localization of intraepithelial neoplasia .

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Equipment Bronchoscopy A dedicated endoscopic system allowing for blue light imaging.

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Two images of different wavelengths (red and green) are captured. Images are processed such that the image on the video monitor allows for normal tissue to be visualized as green and abnormal tissue to be visualized as reddish-brown in color. Inspection is then performed using a standard bronchoscopic technique.

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Initial bronchoscopic examination is performed using conventional WLB. A detailed autofluorescence examination is performed and all abnormalities are graded. Biopsies are then performed either under white light settings of the areas determined to be abnormal, or after (or during) autofluorescence bronchoscopic inspection of the areas determined to be abnormal.

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Chest CT Better for the detection of tumors in the peripheral airways. Although CT is several times more sensitive than standard chest x-ray , lesions smaller than 10 mm that are discovered by this means present a diagnostic challenge.

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On a spiral chest CT, lesions as small as 1 mm can be seen. Despite this sensitivity, preinvasive lung cancers in the central airways are usually not detectable because these early lesions are only a few cell layers thick.

Endobronchial ultrasound (EBUS): 

Endobronchial ultrasound (EBUS)

PowerPoint Presentation: 

Endobronchial ultrasound (EBUS) is a bronchoscopic technique that uses ultrasound to visualize structures within and adjacent to the airway wall. There are two types of EBUS Radial probe EBUS (RP-EBUS) Convex probe EBUS (CP-EBUS)

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Radial ultrasound provides a 360-degree image of the airway wall and surrounding structures external to the airway, perpendicular to the insertion direction of the endoscope. Curvilinear ultrasound provides a 30-degree image of the airway wall and surrounding structures external to the airway, parallel to the insertion direction of the endoscope. Curvilinear EBUS allows physicians to perform TBNA through a curvilinear EBUS bronchoscope.

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EBUS-TBNA is performed under local anesthesia and conscious sedation in an outpatient setting. Radial ultrasound allows for a 360-degree view of the exact location of a lesion in relation to the airway. This allows for more direct and accurate sampling, increasing the diagnostic yield of the procedure.

Transbronchial needle aspiration [TBNA] in the diagnosis and staging of lung cancer: 

Transbronchial needle aspiration [TBNA] in the diagnosis and staging of lung cancer

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Relatively new , quick , safe and painless endoscopy procedure Used in the diagnosis of Endobronchial tumors Submucosal tumors Peripheral masses Mediastinal staging and the Diagnosis of inflammatory and infectious diseases

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In 1983 wang & terry first described the procedure of TBNA for mediastinal lymphnode sampling using flexible bronchoscope

Anatomic considerations: 

Anatomic considerations Anteriorly and to the right of the distal third of the trachea are found the superior vena cava and azygous vein. Directly anterior to the trachea , above the level of the carina lie the innominate and the aortic arch.

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The left pulmonary artery runs anterosuperiorly , in close approximation with the left main bronchus . The right pulmonary artery lies anterior to the right main bronchus and the origin of the upper lobe bronchus.

IASLC lymph node map 2009 : 

IASLC lymph node map 2009

Wang TBNA staging : location of mediastinum and hilar lymph nodes for TBNA(defined by CT scan): 

Wang TBNA staging : location of mediastinum and hilar lymph nodes for TBNA (defined by CT scan)

Lymph node Location: 

Lymph node Location Anterior carina Posterior carina Infront and between proximal portion of right and left main bronchi Behind and between proximal portion of right and left main bronchi,or directly behind rt main bronchus

Lymph node Location: 

Lymph node Location 3. Right paratracheal 4. Left paratracheal (aortic pulmonary window) 5. Right main bronchus Behind superior vena cava and infront of antero lateral aspect of lower trachea near azygous arch Lateral to trachea near tracheal angulation,below aortic arch and above left main pulmonary artery. In front of right main bronchus

Lymph node Location: 

Lymph node Location 6. Left main bronchus 7. Right upper hilar 8. Sub carina In front of left main bronchus In front and between rt upper lobe bronchus and bronchus intermedius Between rt & lt main bronchi, at or near level of rt UL bronchus.

Lymph node Location: 

Lymph node Location 9. Right lower hilar 10. Sub sub carina 11. Left hilar Lateral or in front of bronchus intermedius , at or near level of rt ML bronchus Between bronchus intermedius and left main bronchus, at or near level of rt ML bronchus Between left UL & left LL bronchus.

Wang TBNA staging system: TBNA site for mediastinum & hilar lymphnodes (defined by bronchoscopy): 

Wang TBNA staging system: TBNA site for mediastinum & hilar lymphnodes (defined by bronchoscopy )

Lymphnode Site: 

Lymphnode Site Anterior carina Posterior carina Right paratracheal First & second inter cartilage interspace from lower trachea at about 12-1 0’clock position Posterior portion of carina at about 5-6 0’clock position 2 nd -4 th intercartilagenous interspace of lower trachea at about 3 o’clock position

Lymphnode Site: 

Lymphnode Site 4) Left paratracheal 5) Right main bronchus 1 st or 2 nd intercartilagenous interspace from lower trachea at about 9 o’clock position 1 st or 2 nd intercartilagenous interspace from proximal right main bronchus at about 12 o’clock position

Lymphnode Site: 

Lymphnode Site 6) Left main bronchus 7) Right upper hilar 8) Sub carina 1 st or 2 nd intercartilagenous interspace from proximal left main bronchus at about 12 o’clock position Anterior portion of right upper lobe spur Medial wall of right main bronchus at about 9 o’clock position proximal to level of right upper lobe orifice

Lymphnode Site: 

Lymphnode Site 9) Right lower hilar 10) Sub subcarina 11) Left hilar Lateral or anterior wall of bronchus intermedius at about 3 o’clock position & 12 o’clock positon near or at level of right middle lobe orifice Medial wall of bronchus intermedius at about 9 o’clock position , proximal to level of rt middle lobe orifice Lateral wall of lt LL bronchus at about 9 0’clock, at level of superoir segment orifice of lt LL.

T N M STAGING OF LUNG CANCER (1999-IASLC): 

T N M STAGING OF LUNG CANCER (1999-IASLC)

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T0 - No primary tumor T1 - Tumor </= 3 cm in greatest dimension Surrounded by lung or visceral pleura Not more proximal than the lobar bronchus T1a - Tumor </= 2 cm T1b - Tumor >2 cm but </= 3 cm

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T2 –Tumor > 3 but </= 7 cm or Tumor which invades visceral pleura Involves main bronchus >/= 2 cm distal to the carina Atelectasis / obstructive pneumonia extending to hilum but not involving the entire lung T2a – tumor > 3 but </= 5 cm T2b – tumor > 5 but </= 7 cm

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T3 – Tumor > 7 cm or Directly invading Chest wall Diaphragm Phrenic nerve Mediastinal pleura or Parietal pericardium Tumor in the main bronchus < 2 cm distal to the carina Atelectasis or obstructive pneumonitis of entire lung Separate tumor nodules in the same lobe

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T4 – tumor of any size with invasion of Heart Great vessels Trachea Recurrent laryngeal nerve Esophagus Vertebral body or carina or separate tumor nodules in a different ipsilateral lobe

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N0 – no regional node metastasis N1 – metastasis in ipsilateral peri bronchial and / or peri hilar lymph nodes and intra pulmonary nodes , including involvement by direct extension

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N2 – metastasis in ipsilateral mediastinal and / or sub carinal lymph nodes N3 – metastasis in:- contralateral mediastinal - contralateral hilar, - ipsilateral or contralateral scalene OR supra clavicular lymph nodes

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M0 – no distant metastasis M1 - Distant metastasis -M1a – separate tumor nodules in a contralateral lobe ,or tumor with pleural nodules or malignant pleural dissemination -M1b – distant metastasis

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SPECIAL SITUATIONS T X , N X ,M X –T , N , or M status not able to be assessed Tis - focus of in situ cancer T1∫∫ - superficial spreading tumor of any size but confined to the wall of the trachea or mainstem bronchus .

TNM elements included in stagegroups : 

TNM elements included in stagegroups Ia – T1a,b No Mo Ib – T2a N0 Mo

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IIa – T1a,b N1 M0 T2a N1 M0 T2b N0 M0 IIb – T2b N1 M0 T3 N0 M0

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IIIa – T1-3 N2 M0 T3 N1 M0 T4 No,1 M0 IIIb – T4 N2 M0 T1-4 N3 M0 IV – T any N any M1a,b

Approach to the management of lung cancer: 

Approach to the management of lung cancer

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FOUR OBJECTIVES 1) How to perform the diagnosis 2) How to eliminate other diseases 3) How to treat the patient 4) Can the patient tolerate surgery

How to perform the diagnosis: 

How to perform the diagnosis Neg. Pos. Clinical symptoms Clinical signs Hemoptysis Chest radiograph Stop Fiberoptic Bronchoscopy CT scan Transthoracic Biopsy Mediastinoscopy Exploratory thoracotomy Pretreatment Work-up Clinical and radiological Follow-up Stop

How to perform the diagnosis: 

How to perform the diagnosis Neg. Pos. Clinical symptoms Clinical signs Hemoptysis Chest radiograph Stop Fiberoptic Bronchoscopy CT scan Transthoracic Biopsy Mediastinoscopy Exploratory thoracotomy Pretreatment Work-up Clinical and radiological Follow-up Stop

How to eliminate other diseases: 

How to eliminate other diseases Pulmonarymetastasis . Nodular opacities . Lymphangitis Hematologic disease Lymph node enlargement Benign tumor . Nodular opacity . Atelectasis Tuberculosis Infiltrative & cavitating opacities Pneumonia Nonretractile opacity With Alveolar bronchogram Pulmonary infarction Sub pleural opacity With pleural reaction Pulmonary hematoma . Nodular opacity . Alveolar condensation BRONCHOGENIC CARCINOMA

How to treat the patient: 

How to treat the patient NON SMALL CELL LUNG CANCER Stages I , II , IIIa --- Treated by SURGERY Stages I , II , IIIa --- Cured by SURGERY ± RADIOTHERAPY Stages IIIa , IIIb --- RADIOTHERAPY ± CHEMOTHERAPY Stages IIIb , IV --- CHEMOTHERAPY alone

How to treat the patient: 

How to treat the patient SMALL CELL LUNG CANCER Limited Disease --- CHEMOTHERAPY + RADIOTHERAPY Extensive disease --- CHEMOTHERAPY

PowerPoint Presentation: 

Can the patient tolerate surgery NSCL cancer patient Clinically operable Stage I , II , IIIa Is there any other unstable medical condition No PFT FEV > 2 lit SURGERY No Surgery would impair Pulmonary function Yes Surgery impossible Corticosteroid treatment FEV < 2 liters FEV < 1.5 liters Surgery impossible Yes FEV 1.5-2 liters Perfusion scan Exercise test Surgery possible after Medical treatment PFT

SURGICAL MANAGEMENT OF LUNG CANCER: 

SURGICAL MANAGEMENT OF LUNG CANCER

NON SMALL CELL LUNG CANCER: 

NON SMALL CELL LUNG CANCER SURGERY -- Best treatment for this group The fitness of the patient under going surgery is also important

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PRE OPERATIVE EVALUATION VERY LOW RISK – Normal cardiac function & ECG Normal arterial BP FEV1 70% or more

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MODERATE RISK – Coronary artery disease Arrythmias Systemic hyper tension Myocardial dysfunction Hypoxia with normal Pa CO2 FEV1 35-70 %.

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VERY HIGH RISK – Congestive cardiac failure Ventricular arrhythmias Uncontolled malignant hypertension Recent myo cardial infarction Pa CO2 > 45 mm Hg FEV1 35% or less Pulmonary hypertension.

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Resection is the best treatment of localised , non small cell lung cancer . The standard methods are pneumonectomy & lobectomy

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Lesser or limited operations include wedge resection , segmental resection , non anatomic limited resection , & sleve lobectomy . The lesser resections are usually indicated in patients with poor cardio pulmonary reserve , & tumors in the T1 stage and are usually N0.

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Extended resections -- In stage IIIa disease with T3 N2,3 disease superior sulcus tumor. Tumors <2cm distal to carina – sleve lobectomy or pneumonectomy . Post operative radiotherapy , particularly in superior sulcus tumors have shown improved results.

RADIATION THERAPY IN LUNG CANCER: 

RADIATION THERAPY IN LUNG CANCER

Conventional fractionation: 

Conventional fractionation 5 fractions / week Dose for fraction ranging between 180 -200 cGy . 6-7 weeks

Altered fractionation: 

Altered fractionation A ] HYPER FRACTIONATION More than 1 fraction per day Smaller fractional dose [110 -150 cGy ] Same overall time Total dose 10- 15% higher

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B ] ACCELERATED FRACTIONATION Conventional dose fractions are used more than once daily to shorten the overall treatment duration. C ] ACCELERATED HYPER FRACTIONATION Decrease in the dose per fraction Shortening of overall treatment duration Dose per fraction – 125 cGy -180 cGy

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D ] CONTINOUS HYPER FRACTIONATED ACCELERATED RADIOTHERAPY {CHART} Involves acceleration where more than one treatment is given per day on every treatment day to both the large & small volumes. Overall treatment duration reduced to 12 days with no weekend gaps.

PowerPoint Presentation: 

At the beginning the treatment was given @140 cGy per fraction for 36 fractions there by giving a total dose of 5040 cGy of which 4200 cGy per 30 fractions were given to large volume and 840 cGy per 6 fractions were given to the small volume . Later on the fraction size was increased to 150 cGy per fraction , 3 times daily to a total dose of 5400 cGy of which 4200 cGy per 28 fractions were given to the large volume and 1200 cGy per 8 fractions to the small volume

Radiation therapy in NSCLC: 

Radiation therapy in NSCLC

PowerPoint Presentation: 

Surgery is treatment of choice for NSCLC Radiation therapy is used either alone or in the form of post operative or preoperative radiation in curative settings. Radiation plays an important role in the palliation of locally advanced or metastatic disease , rather it is the only modality for such patients

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Radical or curative radiation Post operative radiation Pre operative or neo adjuvant radiation Chemoradiation Palliative radiation

Radical or curative radiation: 

Radical or curative radiation Pneumonectomy can be performed in a fraction of these patients (35% ) , but 75% of these patients with respectable carcinoma die from metastasis undetected at the time of surgery. Radiotherapy fails not only for this same reason , but also from frequent non sterilization of the primary lesion. Ocassionally a patient is cured by irradiation or by surgery.

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AIM To deliver a tumorisidal dose to the primary tumor and to locoregional areas of spread. The treatment volume should therefore , include the radiographically visible tumor , hilar , and mediastinal lymph node ares , with a margin allowing for the microscopic extension of tumor.

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Definitive radical or curative radiation is indicated in Resectable but : medical contra indication for surgery patient who refuses surgery critical organ located near the tumor Non resectable : Stage II , IIIA , and IIIB disease Patients with small localized residual / recurrent tumor following surgery

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TREATMENT PLANNING Patient is made to lie down in Rx position Fields of radiation are selected and marked Verification of Rx fields is done on SIMULATOR Images from simulator are transferred to TPS Iso dose distribution is caliculated

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Once the dose time and fractionation is decided the patient is treated on either LINEAR ACCELERATOR with 6 – 10 MeV X – ray beam or COBALT – 60 machine.

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RADICAL RADIATION DOSAGE 60 – 70 Gys delivered in 6 – 7 Wks in 30 – 35 fractions using conventional fractionation where dose per fraction does not exceed 2 Gy . Altered fractionation regimen in the form of hyper fraction or accelerated hyper fraction has also been used with marginal improvement in local control and therefore , to be used only in special situations.

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RESULTS EXCELLENT RESULTS in the patients whose tumor are Smaller than 2 – 4 cm In patients with excellent performance status In those given tumor doses 60 Gy or more.

POST OPERATIVE RADIATION: 

POST OPERATIVE RADIATION Indicated for positive or close margins following radical surgery . Also indicated in operable patients with T2 – T3 lesions Microscopically hilar or mediastinal lymph nodes Patients with unfavourable histology

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DOSAGE IN POST OPERATIVE RADIOTHERAPY A dose of 60 – 66 Gys is usually delivered in 6 – 6 ½ Wks RESULTS Has definitively increased the control rate of stage II and III cases. But have produced NO BENEFIT ON SURVIVAL .

PRE OPERATIVE or NEO ADJUVANT IRRADIATION: 

PRE OPERATIVE or NEO ADJUVANT IRRADIATION Indications Equivocally operable or locally advanced inoperable tumors. To make the tumor operable To decrease post operative recurrences

CHEMO RADIATION: 

CHEMO RADIATION INDICATIONS To improve the results To increase the resectabality To increase the survival following surgery To increase the control rate of curative radiation To achieve higher palliation in locally advanced lesions

PowerPoint Presentation: 

Chemotherapy is used either prior to radiation or during the radiation Therefore , chemoradiation has been used in stage I to stage IIIA disease Chemotherapy is usually given 3 – 4 months prior to radical radiation to the dose of 45 – 60 Gy . Considered treatment of choice for locally advanced disease .

PALLIATIVE RADIATION: 

PALLIATIVE RADIATION Greatly improves the quality of remaining life Is aimed at growth restraint , rather than at tumor ‘sterilizations’. Resolution of treated symptoms for the duration of patients life is the aim

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Indicated in advanced local disease for palliation of symptoms like Haemoptysis Cough Dyspnoea Pain due to chest wall infiltration or brachial plexus Dysphagia & Hoarseness of voice.

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DOSAGE 30 Gy in 10 fractions Or 20 Gy in 5 fractions Or 7.5 – 10 Gy in single fraction depending up on the extent and site of the disease

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For SVC syndrome short course radiation dose of 20 Gy in 5 fractions or 30Gy in 10 fractions give best palliation . For extra thoracic bone , lymphnode deposits ,brain metastasis and spinal cord compression a dose of 8 Gy in single fraction or 20 Gy in 5 fractions is most ideal.

INNOVATIVE RADIATION APPROACHES: 

INNOVATIVE RADIATION APPROACHES 3 Dimensional conformal radiotherapy Intensity modulated radiation therapy Gated radio therapy stereotactic radiotherapy Neutron therapy Interstitial brachytherapy Intra luminal brachytherapy Intra operative radiotherapy

complications: 

complications ACUTE: 3 RD WEEK - esphagitis,cough,skin recetion,fatigue LATE: 2- 3 yrs later -radiation pneumonitis , -Pulmonary fibrosis esophageal stenosis,fistula cardiac damage spinal cord damage- radiculopathies

RADIOTHERAPY IN SCLC: 

RADIOTHERAPY IN SCLC

PowerPoint Presentation: 

SCLC is a rapidly proliferating , biologically aggressive form of lung cancer that has a short survival with out treatment Chemotherapy is the main stay of treatment

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INDICATIONS Mainly in patients with limited stage disease Those who respond favourably to chemotherapy For palliation in patients presenting with extensive disease

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Concomitant Chemotherapy & Thoracic irradiation Therapy for limited disease SCLC includes radiation & systemic chemotherapy The standard chemotherapy is ETOPOSIDE & either CISPLATIN administered concomitantly with radiotherapy given once or twice daily. PACLITAXEL has demonstrated efficacy in extensive disease SCLC.

PowerPoint Presentation: 

A marginal advantage is seen in initial radiotherapy versus delayed radiotherapy Multi agent chemotherapy for 4 – 6 cycles followed by thoracic irradiation in all patients with no distant metastasis on staging re evaluation. Usual dose in 50 Gy to the patients who have achieved complete response and 60 – 66 Gy to those with partial response in 1.8 to 2 Gy fraction.

MANAGEMENT OF LUNG CANCER CHEMOTHERAPY : 

MANAGEMENT OF LUNG CANCER CHEMOTHERAPY

Small cell lung cancer: 

Small cell lung cancer Considered to be a systemic disease because of early metastasis. Therefore , chemotherapy is the treatment of choice. > 95% of patients will be classified as having stage IIIb or IV disease. Fortunately respond well with chemotherapy. Etoposide basd - superior

PowerPoint Presentation: 

Ideal therapeutic goal To develop a treatment protocol which produces the highest percentage of long term disease free survival (cure) with the less possible morbidity due to the therapy itself.

Active agents against small cell lung cancer: 

Active agents against small cell lung cancer Drug Response rate (%) Ifosfamide 50 Teniposide 50 Etoposide 40 Carboplatin 40 Cyclophosphamide 40 Vincristine 35 Methotrexate 35 Doxorubicin 30

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Drug Response rate (%) Hexamethylmelanin 30 Vinblastine 30 Vindesine 30 Cisplatin 15 Lomustine 15

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Drug Response rate (%) NEWER DRUGS Taxanes Paclitaxel 34-41 Docitaxel 28 Captothecins CPT – 11 47-78 Topotecan 35-39 Gemsitabine 30

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Combination therapy is superior to single agents. The duration of treatment is uncertain. Most trials are maintaining chemotherapy for periods of 6 to 12 months.

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After about 3 to 6 months a restaging is done including a liver and bone marrow and bronchoscopy . If there is complete remission, treatment can be stopped after 6 months. Even with complete remission after one year of therapy , about 1/3 of all patients will relapse.

Means to improve the results of chemotherapy: 

Means to improve the results of chemotherapy Use of alternating non-cross-resistant chemotherapy to delay or prevent the emergence of drug resistance during therapy Administration of drugs according to the cell cycle kinetics.

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Incorporation of new drugslike JM-8 , JM-9 and VM-26 , having high anti-tumor activity. Intensive high dose chemotherapy with or with out bone marrow rescue.

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Simultaneous use of synergistic compounds. Use of drugs according to the tumor cell culture and sensitivity. Use of immunostimulants . Use of anticoagulants.

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Regimens Dose and Schedule Cyclophosphamide 1 gm/m2 iv day 1 q 4 weeks CCNU 70 mg /m2 PO day 1 q 4 weeks Vincristine 1.3 mg / m2 iv day 1 q 4 weeks except weekly for the first 4 weeks VP – 16 70 mg / m2 PO daily on days 2 – 5 q 4 week

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Regimens Dose and Schedule 2) Cyclophosphamide 1.5 g/m2iv q 3 weeks Adriamycin 40mg/m2 q 3 weeks Vincristine 2 mg/m2 q 3 weeks 3) VP – 16 50 mg/m2 iv daily X 5 q 3 weeks Adriamycin 45 mg/m2 iv X 1 q 3 weeks Cyclophosphamide 1 gm/m2 iv q 3 weeks

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Regimens Dose and Schedule 4) Ifosfamide 5 gm/m2 iv day 1 or 1.5 gm/m2 day 1 – 5 VP – 16 100 – 120 mg/m2 iv day 1 – 3 5) Carboplatin 300 mg/m2 iv day 1 VP – 16 100 mg/m2 iv days 1 – 3 6) Ifosfamide 5 gm/m2 iv day 1 Etoposide (VP-16) 100 mg/m2 iv days 1 – 3 Carboplatin 400 mg/m2 iv day 1

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Associated complications like SVC obstruction can be treated with chemotherapy alone with similar results to that of radiotherapy. If not effective – palliative radiotherapy may be tried Rx of primary CNS metastasis – systemic chemotherapy + radiotherapy. Most patients relapse within 10-12 months.

Non small cell lung cancer: 

Non small cell lung cancer Role of chemotherapy is undefined. Response rate was significantly lower for single agent chemotherapy than for combination chemotherapy. Best results were obtained with regimens containing cisplatin , vindesine , vinblastine , mitomycin c , ifosfamide , doxorubisin , and etoposide . Cisplatin based- superoir

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Regimens Dose and Schedule 1) Cisplatin 120 mg/m2 day 1 and 29 then every 6 weeks iv + Vinblastine 6 mg/m2 weekly X 5 then q 3 weeks iv or Vindesine 3 mg/m2

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Cisplatin as above + Vindesine as above + Mitomycin C 8 mg/m2 on day 1 , 29 , and 71

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Regimens Dose and Schedule Mitomycin C 6 mg/m2 day 1 iv Ifosfamide 3 gm/m2 iv infused over 3 hrs day 1 Cisplatin 50 mg/m2 iv infused over 1 hr day 1. THE CYCLE IS REPEATED EVERY 3 WEEKS

Biological agents: 

Biological agents Retiniods Interferons Interleukins LAK cells MAB EGFR inhibitors VEGF inhibitors Explored as alternatives to traditional chemotherapies

Methods for measuring quality of life: 

Methods for measuring quality of life

Karnofsky scale ECOG / WHO scale: 

Karnofsky scale ECOG / WHO scale

Karnofsky scale: 

Karnofsky scale Normal ; no complaints or evidence of disease 100 Able to carry on normal activity ; minor signs 90 or symptoms of disease Normal activity with effort ; some signs or 80 symptoms of disease Cares for self ; unable to carry on normal 70 activity or to do active work

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Requires occasional assistance , but is able to 60 care for most personal needs Requires considerable assistance and 50 frequent medical care Disabled ; requires special care and assistance 40 Severely disabled ; hospitalization is indicated 30 although death not immitent

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Very sick ; hospitalization and active 20 supportive treatment necessary Moribund ; fatal processes progressing 10 rapidly

ECOG / WHO scale: 

ECOG / WHO scale Able to carry out normal activity 0 Restricted in physical strenuous activity but 1 ambulatory Ambulatory and capable of self care 2 unable to work Capable of only limited self care , confined to 3 bed or chair > 50% of working hours Completely disabled ; cannot carry out self care 4

PROGNOSIS: 

PROGNOSIS

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In all types of lung cancers Over all survival 5 year after diagnosis is 5 – 15% Duration of survival depends on Size of the tumor at diagnosis Its doubling time . Small cell carcinoma – 50 days Squamous and large cell – 100 days Adenocarcinoma – 180 days

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NON SMALL CELL CARCINOMA 5 – year survival rates – 4 to 7 % , irrespective of whether the patient received surgery , radiotherapy or chemotherapy. Stage –I tumors when treated surgically – 30 – 60 %. Stage –II tumors when treated surgically – 20 – 40 %.

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Stage IIIA IIIB Survival at 12 months – 37.7 % 31.8 % 24 months – 12.7 % 10.8 % 60 months – 6.1 % 3.9 % irrespective of treatment In stage IV disease 1 year survival is 19.8 % 2 year survival is 5.4 %

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SMALL CELL CARCINOMA Medial survival for untreated patients – 2.8 months For limited disease – 3.1 months For more extensive disease – 1.4 months After aggressive chemotherapy – 8 – 14 months

Extrapulmonary syndromes associated with lung tumors: 

Extrapulmonary syndromes associated with lung tumors

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HYPERCALCEMIA OF MALIGNANCY HYPONATREMIA OF MALIGNANCY ECTOPIC ACTH SYNDROME ACROMEGALY

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HEMATOLOGIC SYNDROMES NEUROLOGIC SYNDROMES CANCER-ASSOCIATED RETINOPATHY LAMBERT-EATON SYNDROME

HYPERCALCEMIA OF MALIGNANCY: 

HYPERCALCEMIA OF MALIGNANCY Most common paraneoplastic syndrome. In only 1 percent of patients when first seen. 10 to 20 percent of patients during the course of their disease.

HYPERCALCEMIA OF MALIGNANCY: 

HYPERCALCEMIA OF MALIGNANCY Lung cancer is the most common solid tumor . 30 to 40 percent of all paraneoplastic cases. Commonly seen in patients with squamous cell carcinoma of the lung. Uncommonly with adenocarcinoma , and very rarely in small-cell lung cancer.

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Mostly (80-90%)by the ectopic production of parathyroid hormone–related peptide ( PTHrP ) by tumor cells.

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PTHrP binds to PTH receptors in the bone and kidney Increased osteoclastic bone resorption Decreased bone formation Decreased calciuria hypercalcemia .

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Low Renal α- hydroxylase activity suppressed 1,25-dihydroxyvitamin D3 levels Raised in patients with primary hyperparathyroidism.

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Thirst Malaise Fatigue Confusion Anorexia Lethargy Polyuria Coma Constipation Death Nausea Vomiting

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Treatment of the underlying cancer. Intravenous saline plus furosemide diuresis . Subcutaneous calcitonin in severe cases. Mithramycin and long-acting biphosphonates , such as pamidronate , for long-term control of hypercalcemia .

HYPONATREMIA OF MALIGNANCY: 

HYPONATREMIA OF MALIGNANCY More than 90 percent with small-cell lung cancer.

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Small-cell lung cancer Ectopic production of AVP (SIADH) Inhibiting free-water excretion in the distal tubule Hyponatremia Ectopic production of ANP may also play a role

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Syndrome develops over a prolonged period . The symptoms do not typically occur. Most frequently diagnosed as a laboratory abnormality.

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Mild hyponatremia ( > 120 mEq /ml)-- headache, difficulty in concentrating, nausea, weakness, and fatigue. More acute hyponatremia -- confusion, lethargy, seizures, coma, and death.

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Rx: Demeclocycline 600 to 1200 mg orally per day Blocks the action of AVP on the renal tubule Inducing diabetes insipidus Correct the hyponatremia Lithium and Phenytoin can also be used

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In severe, symptomatic hyponatremia I.V. 3 percent hypertonic saline along with I.V. furosemide , is recommended.

ECTOPIC ACTH SYNDROME: 

ECTOPIC ACTH SYNDROME 50 percent of all lung CA cases. Small-cell carcinoma accounts for 80 to 90 % . Carcinoid tumors (10 percent) Bronchial adenocarcinomas (5 percent).

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Fewer than 3 percent of patients with small-cell lung cancer have Cushing’s syndrome at the time of diagnosis. Mostly caused by ectopic production of ACTH by the tumor.

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Small-cell carcinoma or bronchial carcinoid CRH is produced by the cancer cells ACTH production by the pituitary gland ACTH binds to receptors in the adrenal gland Excessive glucocorticoid and mineralocorticoid hormones Cushing’s syndrome.

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Ectopic ACTH production occurs with equal frequency in males and females —unlike Cushing’s syndrome, which has an 8:1 female preponderance. Patients who have slow-growing tumors ( carcinoids ) often present with the clinical features of Cushing’s syndrome: Truncal obesity moon facies striae polyuria polydipsia .

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In contrast, patients with small-cell lung cancer often present with other signs of mineralocorticoid and glucocorticoid excess due to the rapidity of tumor growth: Edema weakness Hypertension hypokalemic alkalosis.

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Diagnosis of ectopic ACTH syndrome Increased 24-h excretion of urinary free cortisol (more than 400 nmol a day) Increased plasma cortisol level (more than 600 nmol /l) Increased plasma ACTH level (over 22 pmol /l), which do not decrease in response to the administration of high-dose dexamethasone .

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Bronchial carcinoids are an exception because, in some tumors, ACTH and cortisol levels have been suppressed by dexamethasone . If dexamethasone suppression test does not establish the diagnosis , a CRH stimulation test or bilateral inferior petrosal vein sampling will provide the definitive diagnosis.

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After CRH infusion Pituitary tumors release increased amounts of ACTH Pituitary-independent lung tumors do not.

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Similarly, in pituitary-dependent Cushing’s syndrome , petrosal vein sampling will reveal a gradient between the level of ACTH in the petrosal vein and the peripheral concentration. In contrast, patients in whom ACTH is ectopically produced demonstrate no gradient between the petrosal vein and the peripheral blood.

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Treatment Remove the source by chemotherapy , with or without irradiation, for patients with small-cell lung cancer Surgical resection and/or radiation for carcinoid tumors

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Ketoconazole inhibits steroidogenesis at both adrenal and gonadal sites. Metapyrone and aminoglutethimide also inhibit adrenal steroid synthesis. Octreotide , a somatostatin analogue, can suppress ectopic ACTH production .

ACROMEGALY: 

ACROMEGALY Carcinoid tumors of the lung and intestine -- 70 percent of cases. Ectopic production of growth hormone–releasing hormone (GHRH) by tumor cells in most patients. A minority of tumors produce growth hormone.

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GHRH gene expressed by the cancer cells A 40– or 44– amino acid peptide secreted Binds to receptors in the pituitary gland Production of excessive amounts of GH Acromegaly

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Immunoreactive GHRH -- In many bronchial carcinoids and small-cell lung cancers Acromegaly in a minority of these patients.

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Ectopic GHRH production may not cause clinically evident acromegaly because: (1) The tumor produces inadequate amounts of GHRH (2) The hormone is synthesized but not secreted (3) The rapid progress of the malignancy prevents the full development of clinical features of acromegaly .

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The earliest features of GH excess Hypertrophy of the extremities and face Thickened leathery skin Prominent skin folds Increased skin pigmentation, and hair growth. Bony changes, hypertension, and diabetes mellitus are later, less common findings.

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Diagnosis Increased levels of GHRH and IGF-1 in the patient’s plasma The absence of a pituitary tumor The demonstration of GHRH or GH in tumor tissue by immuno histo chemistry or mRNA expression studies.

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Treatment Removal of the GHRH- or GH-secreting tumor. Somatostatin analogue octreotide or bromocriptine .

HEMATOLOGIC SYNDROMES: 

HEMATOLOGIC SYNDROMES Granulocytosis Non–small-cell lung cancer -- most common. Twenty percent of patients with non–small-cell lung cancer have granulocytosis , with absolute white blood counts ranging from 10,100 to 25,000 (normal range is 4000 to 10,000).

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Virtually all patients are asymptomatic. Diagnosis -- Increased WBC with neutrophils predominance , in the absence of non neoplastic causes. An increased leukocyte alkaline phosphatase score and a normal bone marrow are consistent with this diagnosis.

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Thrombocytosis In 40 % of patients with both non–small-cell and small-cell tumors. Increased levels of IL-6 have been demonstrated. The recent identification of the thrombopoietin gene as a role.

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Always asymptomatic Do not have an increased incidence of thromboembolism . Diagnosis by an increased platelet count (above 500,000/mm2) in a patient with newly diagnosed lung cancer.

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Thromboembolism Seen in 20% of patients with lung cancer during the course of their disease. Twenty percent of patients with recurrent idiopathic venous thrombosis are found to have an underlying diagnosis of cancer.

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Causes of thrombosis in patients with lung cancer Disseminated intravascular coagulation (DIC) Trousseau’s syndrome Nonbacterial thrombotic endocarditis Obstruction of great vessels.

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Oral warfarin therapy is appropriate If there are recurrent thromboses long-term subcutaneous heparin is more efficacious.

NEUROLOGIC SYNDROMES: 

NEUROLOGIC SYNDROMES Encephalomyelitis Cerebellar degeneration Retinopathy Opsoclonus / myoclonus Lambert-Eaton syndrome Most commonly by smallcell lung cancer . Mostly by an autoimmune response directed at antigens that are shared by the cancer cells and normal neural tissue.

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Encephalomyelitis/ Subacute Sensory Neuropathy In more than 70 percent of small-cell lung cancer. A specific antibody, anti- Hu , which reacts with the HuD antigen expressed by lung cancer cells and neuronal tissues, has been associated.

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One-half of patients undergo progressive sensory loss in the hands and feet. Others present with a limbic encephalopathy characterized by memory loss, behavioral changes, and seizures. Focal myelopathy with weakness, brain stem signs ( nystagmus , dysarthria ), and autonomic nervous system dysfunction also occur in patients with this syndrome.

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CT scans are typically normal in these patients MRI studies may show increased T2 signal in affected areas of the brain. Pathologic examination of brain biopsies show inflammatory infiltrates and neuronal destruction in the brain stem, hippocampus, spinal cord, and dorsal root ganglia

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Immunosuppressive therapy with corticosteroids and plasmapheresis is effective in only 10 to 20 %. Patients severely affected by the anti- Hu syndrome can die from neurologic sequelae (e.g., cardiovascular collapse).

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Paraneoplastic Cerebellar Degeneration Noted in patients with small-cell lung cancer. Considered to have the anti- Hu syndrome Frequently go on to develop encephalitis or sensory neuropathy.

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Opsoclonus and Myoclonus Opsoclonus -- Involuntary rapid conjugate eye movements in vertical and horizontal directions. Often associated with myoclonus in patients with solid tumors. Associated with both small-cell and non–small-cell lung cancer .

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A specific antibody called anti- Ri has been identified. The anti- Hu antibody has been identified in some patientswith small-cell lung cancer and opsoclonus / myoclonus . Retinal ganglion cells and their processes are characteristically lost.

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The clinical triad Photosensitivity Ring- scotomata Attenuation of retinal arteriole caliber Highly suggestive of cancer-associated retinopathy

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Symptoms -- Rapid visual loss Night blindness Color loss. Show -- Visual field deficits Disk pallor Cells in the vitreous body Arteriolar narrowing.

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Demonstration of the antirecoverin antibody -- diagnosis. More than half respond with systemic steroid therapy.

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LAMBERT-EATON SYNDROME Reported in up to 5% of patients with small-cell lung cancer. Sixty percent of all patients who present with the Lambert-Eaton syndrome have small-cell lung cancer.

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An IgG autoantibody Binds to calcium channels in motor and autonomic nerve terminals Inhibits acetylcholine release.

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Clinical features : weakness of the pelvic girdle Fatigue Dry mouth Dysarthria Dysphagia Blurred vision Muscle pain Unlike with myasthenia gravis , muscle strength improves with exercise and does not improve with the administration of anticholinesterases (e.g., edrophonium ).

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Treatment of the underlying small-cell lung cancer. If not improved with chemotherapy Immune modulation with azathioprine (2.5 mg/kg per day) Plasma exchange , or Intravenous γ -globulin (400 mg/kg per day for 5 days) has been shown to induce remissions. 3,4-Diaminopyridine in doses of 10 to 100 mg a day has also been used successfully.

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