This document provides information on primary pulmonary neoplasms (lung cancer). It discusses the epidemiology and causes of lung cancer, including the major risk factor of cigarette smoking. It then covers the histologic classification of lung cancers, distinguishing between non-small cell lung carcinoma (NSCLC) and small cell lung carcinoma. Within NSCLC, it describes the characteristics and radiologic manifestations of the main subtypes: squamous cell carcinoma, adenocarcinoma, and other rare types. Key precursor lesions like atypical adenomatous hyperplasia and diffuse idiopathic pulmonary neuroendocrine cell hyperplasia are also summarized.
Management of Early Breast Cancer (by Dr. Akhil Kapoor)Akhil Kapoor
Comprehensive discussion on Management of Early Breast Cancer along with NCCN guidelines.
Slides prepared by Dr. Akhil Kapoor
(Resident, Department of Radiation Oncology,
Acharya Tulsi Regional Cancer Treatment & Research Institute, Bikaner, Rajasthan, India
Target Audience: Oncology fellows and Oncologists
Carcinoma of unknown primary is a challenging scenario often encountered in Oncology practice. This slide presentation discusses favorable and unfavorable presentations of CUP and it's management
In this presentation our agenda is
Brief introduction
Radiological Modalities
Radiological Features
Radiological Imaging Of Complications of lung cancer.
I followed Dahnert and try to describe all findings in lung cancer.
Hope it will prove an atlas in Lung cancer imaging.
Non–small cell lung cancer (NSCLC) accounts for approximately 85% of all lung cancers. Histologically, NSCLC is divided into adenocarcinoma, squamous cell carcinoma (SCC) (see the image below), and large cell carcinoma. Small cell lung cancer (SCLC), previously known as oat cell carcinoma, is considered distinct from other lung cancers, which are called non–small cell lung cancers (NSCLCs) because of their clinical and biologic characteristics.
Management of Early Breast Cancer (by Dr. Akhil Kapoor)Akhil Kapoor
Comprehensive discussion on Management of Early Breast Cancer along with NCCN guidelines.
Slides prepared by Dr. Akhil Kapoor
(Resident, Department of Radiation Oncology,
Acharya Tulsi Regional Cancer Treatment & Research Institute, Bikaner, Rajasthan, India
Target Audience: Oncology fellows and Oncologists
Carcinoma of unknown primary is a challenging scenario often encountered in Oncology practice. This slide presentation discusses favorable and unfavorable presentations of CUP and it's management
In this presentation our agenda is
Brief introduction
Radiological Modalities
Radiological Features
Radiological Imaging Of Complications of lung cancer.
I followed Dahnert and try to describe all findings in lung cancer.
Hope it will prove an atlas in Lung cancer imaging.
Non–small cell lung cancer (NSCLC) accounts for approximately 85% of all lung cancers. Histologically, NSCLC is divided into adenocarcinoma, squamous cell carcinoma (SCC) (see the image below), and large cell carcinoma. Small cell lung cancer (SCLC), previously known as oat cell carcinoma, is considered distinct from other lung cancers, which are called non–small cell lung cancers (NSCLCs) because of their clinical and biologic characteristics.
Presentation about lung cancer, form, types, classification, treatment. A lot of anatomical and histological pictures accompanied with small and precised informations about every type of lung cancer.
Tumors of lung with its 2015 WHO classification along with cytological evidences to rule out various differential diagnosis. The difference between small biopsy and resected specimen terminology has been briefed in a precise manner.
Cancertame | Lung Cancer | Symptoms, Stages, Diagnosis, Risk Factors, and Met...Cancertame Private Limited
What is Lung Cancer? Lung Cancer is an abnormal growth of cells in one or both lungs of the body. Learn more about Lung Cancer from our website.
For more information: www.cancertame.com
Email us at: support@cancertame.com
Read article at: https://www.cancertame.com/in/articles-list
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
2. EpidemiologyEpidemiology
A common malignancy.
Incidence : in men decreasing
(102 per 100,000 in 1984 & 73.6 in 2004).
-in women increasing since 1960s; rate slowed in
1990s , now approaching a plateau
(50.2 per 100,000 in 2004).
Annual mortality rate : in men - decreased since 1990s by
approximately 1.9% annually,
: in women - approaching a plateau
after increasing for several decades.
Remains one of the leading causes of cancer-related deaths in
men in India and both men and women in the United States.
3. CausesCauses
cigarette smoking:cigarette smoking: strongest risk factor (attributable to up to 90% of lung
cancers in men and 80% in women)
- The risk directly proportional to duration & number of cigarettes smoked.
- Nearly all cases of squamous cell and small cell carcinoma are related to cigarette
smoking
- Adenocarcinoma is the predominant cell type in non-smokers (although its
association with tobacco smoking is increasing)
Involuntary smoke exposure (passive smoking):Involuntary smoke exposure (passive smoking): an excess risk of 20% for
women and 30% for men among never-smokers.
Environmental and occupational exposures:Environmental and occupational exposures: to particulate and chemical
substances. Exposure to the naturally occurring radioactive gas radon, both in
homes and in mines, is the most important risk factor after cigarette smoking.
- Asbestos, arsenic, chloromethyl ethers, chromium, isopropyl oil, mustard gas,
nickel, beryllium, chloroprene, vinyl chloride, and various smelting by-products such
as lead and copper.
Genetic susceptibility:Genetic susceptibility: an important factor, independent of smoking
- gene mutations, such as TP53 and KRAS, are common in lung cancer,
- strong association between KRAS mutations in adenocarcinoma
- mutations of the epidermal growth factor receptor gene appear to have a strong
association with adenocarcinoma (particularly BAC subtype)
4. Histologic ClassificationHistologic Classification
Two major histologic categories:
i) non–small cell lung carcinoma (NSCLC)
ii) small cell lung carcinoma (SCLC)
NSCLC subdivided into histologic types (such as squamous
cell, adenocarcinoma, and large cell), according to the most
differentiated portion of the tumor.
Many tumors composed of more than one type, definitive
diagnosis requires a resected specimen.
NSCLC also graded as well, moderately or poorly
differentiated, according to the least differentiated feature.
Additionally, tumors with immunohistochemical or
ultrastructural features of neuroendocrine differentiation are
collectively referred as NSCLC with neuroendocrine
differentiation.
10. Histologic Classification of Lung TumorsHistologic Classification of Lung Tumors
(By WHO)
i) Epithelial Tumors
A) Benign
Papilloma
Adenoma
B) Malignant
Preinvasive lesions
- Squamous carcinoma in situ
- Atypical adenomatous hyperplasia
- Diffuse idiopathic pulmonary neuroendocrine cell hyperplasia
Non small cell carcinoma
Squamous cell carcinoma
- Variants: Papillary, Clear cell, Small cell, Basaloid
Adenocarcinoma
- Variants: Acinar, Papillary, Bronchioloalveolar, Mixed
subtype
Solid adenocarcinoma with mucin production
11. Atypical AdenomatousAtypical Adenomatous
HyperplasiaHyperplasia Considered a precursor of adenocarcinoma
Localized proliferation of atypical cells lining alveoli and
respiratory bronchioles
Typically less than 5 mm in diameter
Located peripherally in the lung
Most frequently diagnosed in patients with primary non–small cell
carcinoma, especially adenocarcinoma.
Not significantly correlated with gender, age, smoking status,
familial history of malignancy, or preceding malignancy.
Radiologically: AAH manifests as well-circumscribed solitary or
multifocal ground-glass nodular opacities (few mm to 2 cm)
Tend to remain stable for several months to years.
Because of similar radiologic manifestations, CT differentiation
between AAH and adenocarcinoma is difficult, and resection is
usually required for a definitive diagnosis.
12. Histologic Classification of Lung TumorsHistologic Classification of Lung Tumors
(By WHO)
i) Epithelial Tumors
A) Benign
Papilloma
Adenoma
B) Malignant
Preinvasive lesions
- Squamous carcinoma in situ
- Atypical adenomatous hyperplasia
- Diffuse idiopathic pulmonary neuroendocrine cell hyperplasia
Non small cell carcinoma
Squamous cell carcinoma
- Variants: Papillary, Clear cell, Small cell, Basaloid
Adenocarcinoma
- Variants: Acinar, Papillary, Bronchioloalveolar, Mixed
subtype
Solid adenocarcinoma with mucin production
13. (DIPNECH) Diffuse Idiopathic Pulmonary(DIPNECH) Diffuse Idiopathic Pulmonary
Neuroendocrine Cell HyperplasiaNeuroendocrine Cell Hyperplasia
Widespread proliferation of pulmonary neuroendocrine cells or
neuroendocrine bodies within the epithelium of the distal bronchi or
terminal bronchioles.
Uncommon, may be confined to the bronchial and bronchiolar
epithelium, or may extend beyond the basement membrane forming
small localized or diffuse aggregates called tumorlets (<0.5 cm in
diameter) or carcinoids (>0.5 cm).
Fibrous obliterative bronchiolitis and peribronchiolar fibrosis of the
involved airways in 1/3rd
patients.
More frequently in women, mostly in fifth or sixth decade
Typical history of the insidious onset of progressive dyspnea and
chronic nonproductive cough.
Radiologically: Bronchial wall thickening and a mosaic attenuation
pattern (ground-glass opacities and hyperlucent areas) due to
air-trapping. Solitary or multiple nodules (2 to 20 mm in dia.) are an
associated feature.
14. • Diffuse idiopathic pulmonary neuroendocrine cell hyperplasia in a 63-year-
old woman with a chronic history of cough and dyspnea on minimal exertion.
• CT scan shows multiple small bilateral pulmonary nodules (arrows).
• Wedge resection biopsy of the middle lobe revealed carcinoid tumor (5 mm)
and multiple carcinoid tumorlets (<5 mm).
15. Histologic Classification of Lung TumorsHistologic Classification of Lung Tumors
(By WHO)
i) Epithelial Tumors
A) Benign
Papilloma
Adenoma
B) Malignant
Preinvasive lesions
- Squamous carcinoma in situ
- Atypical adenomatous hyperplasia
- Diffuse idiopathic pulmonary neuroendocrine cell hyperplasia
Non small cell carcinoma
Squamous cell carcinoma
- Variants: Papillary, Clear cell, Small cell, Basaloid
Adenocarcinoma
- Variants: Acinar, Papillary, Bronchioloalveolar, Mixed
subtype
Solid adenocarcinoma with mucin production
16. Squamous Cell CarcinomaSquamous Cell Carcinoma
Decreasing in incidence, 30% of all lung cancers.
Typically occur in central bronchi and frequently manifest as
post obstructive pneumonia or atelectasis.
Mucoid impaction, bronchiectasis, and hyperinflation are
uncommon radiologic manifestations.
1/3rd
occur beyond the segmental bronchi and usually range in
size from 1 to 10 cm
Radiologically: More likely to cavitate than the other
histologic cell types of lung cancer. (10% to 30%, commonly in
large peripheral masses and poorly differentiated tumors)
Cavitation is typically eccentric, with thick, irregular
walls, although thin walls may occur in rare circumstances.
Most squamous cell carcinomas grow slowly, and
extrathoracic metastases tend to occur late
NON SMALL CELL LUNG CARCINOMANON SMALL CELL LUNG CARCINOMA
17. A, PA chest radiograph showing
complete atelectasis of the left
upper lobe. Convexity in the lower
portion of the atelectatic lung
(arrow) is the result of a central
mass
B, CT scan confirms an endobronchial
mass (M) that occludes the left upper
lobe bronchus and causes complete
atelectasis of the left upper lobe. Note
the enlarged subcarinal node
(asterisk) due to metastasis
Squamous cell lung cancer manifesting as a central endobronchial
mass
18. A, PA chest radiograph shows a
lobular mass in the right lower
lobe and infrahilar and para
tracheal adenopathy (arrows).
B, CT scan confirms the lobular
mass in the right lower lobe and
infrahilar adenopathy (arrow).
Focal low attenuation within
the mass is consistent with
necrosis.
Squamous cell lung cancer manifesting as a peripheral
mass
19. Histologic Classification of Lung TumorsHistologic Classification of Lung Tumors
(By WHO)
i) Epithelial Tumors
A) Benign
Papilloma
Adenoma
B) Malignant
Preinvasive lesions
- Squamous carcinoma in situ
- Atypical adenomatous hyperplasia
- Diffuse idiopathic pulmonary neuroendocrine cell hyperplasia
Non small cell carcinoma
Squamous cell carcinoma
- Variants: Papillary, Clear cell, Small cell, Basaloid
Adenocarcinoma
- Variants: Acinar, Papillary, Bronchioloalveolar, Mixed
subtype
Solid adenocarcinoma with mucin production
20. AdenocarcinomaAdenocarcinoma
Replaced squamous cell carcinoma as the most frequent cell type, (50% of all lung
cancers).
Typically manifest as peripheral, solitary pulmonary nodules.
Earlier, nodules were typically described having soft tissue attenuation and an
irregular or spiculated margin as a result of parenchymal invasion and an associated
fibrotic response
Now, adenocarcinomas with purely ground-glass, purely solid, or mixed
(ground-glass and solid) attenuation are being detected more often (due to increased
use of CT and screening for lung cancer).
Noguchi classification (based on tumour growth patterns):
- type A: localized bronchioloalveolar cell carcinoma (BAC)
- type B: localized BAC with foci of structural collapse of alveoli
- type C: localized BAC with active fibroblastic proliferation
- type D: poorly differentiated adenocarcinoma
- type E: tubular adenocarcinoma
- type F: papillary adenocarcinoma with a compressive growth pattern
Ground-glass attenuation of nodular opacities is more frequent in types A to C
Soft tissue attenuation is more frequent in types B to F
Likelihood of invasive adenocarcinoma and a more advanced stage of lung cancer
is greater with mixed and solid opacities
21. •CT scan shows a nodule in the right upper lobe (arrow).
•The spiculated margin is typical of lung cancer.
•Note the diffuse emphysema
Adenocarcinoma manifesting as a pulmonary nodule
22. LYMPHANGITIC CARCINOMATOSISLYMPHANGITIC CARCINOMATOSIS :
Although uncommon at presentation, occurs more frequently
with adenocarcinoma and typically manifests radiologically as
thickening of interlobular septa or multiple small
pulmonary nodules.
Intrathoracic metastases to hilar and mediastinal nodes are
present more often with more centrally located
adenocarcinomas
A & B : Thin-section CT scans show thickening of the bronchial walls
and interlobular septa (arrowheads) in the left lung. Nodularity of the
septa is suggestive of malignancy.
23. BRONCHIOLOALVEOLAR CELL CARCINOMABRONCHIOLOALVEOLAR CELL CARCINOMA
(BAC)(BAC):
It is uncommon (<4% of all lung cancers), However, incidence
has increased over the past 2 decades
younger age distribution, higher incidence in never-smokers
and women, and typically more indolent course.
A diverse group of malignancies that share the pathologic
feature of lepidic growth - spread along alveolar septa
without associated lung destruction.
In addition, there is absence of stromal, vascular, or
pleural invasion.
Presentation can be either solitary or multifocal as origin of
BAC is either monoclonal (with multifocality due to
dissemination by aerosolization, intrapulmonary lymphatics, and
intra-alveolar growth) or polyclonal (with multifocality due to
de novo tumor growth at multiple sites
24. Manifestations – a solitary, peripheral pulmonary nodule (43%)
– air space disease (30%),
– and multiple nodules (27%)
(a combination of manifestations may be present in a single patient)
Solitary pulmonary nodules - typically located peripherally, can remain
stable in size for many years.
Morphologically, BAC nodules can be purely ground-glass, mixed (ground-
glass and solid), or solid in attenuation on CT which correspond to biologic
activity : low activity for ground-glass attenuation
invasive for solid opacities
Most pure BAC nodules are mixed with <30% of solid component (shows
collapsed alveoli.
Cystic disease or cavitation is uncommon (<7%) but occurrence of multiple
small, focal, low-attenuation regions (pseudocavitation) or air-bronchograms
within the nodule is occasionally useful in suggesting the diagnosis.
The diffuse form may present as multiple nodules (usually small, typically
ground-glass in attenuation, occasionally cavitary), ground-glass opacities, or
opacities resembling pneumonia (Mostly combination of these).
Hilar and mediastinal adenopathy and pleural effusions are uncommon
25. •CT scan shows a well-marginated ground-glass opacity in the left upper
lobe (arrow).
Bronchioloalveolar cell carcinoma (BAC) manifesting
as
solitary pulmonary nodule
26. •CT scan shows small pulmonary nodules and ground-glass opacities
(Cavitary nodules with central areas of cavitation are occasionally
referred to as the “Cheerio” sign)
Bronchioloalveolar cell carcinoma manifesting as
multiple pulmonary nodules
27. Bronchioloalveolar cell carcinoma opacities mimicking pneumonia
A, PA chest radiograph shows a poorly
marginated, homogeneous,
consolidative opacity in the right
lower lobe.
B, CT scan confirms right lower
lobe consolidation and reveals
ground-glass opacities in the
right lower lobe. CT scan also
revealed diffuse ground-glass
opacities in the middle lobe (not
shown).
28. CT scan shows an opacity in the right upper lobe that resembles
pneumonia, as well as numerous small solid and ground-glass nodules in
the right lung
Bronchioloalveolar cell carcinoma manifesting as nodules
and consolidation.
30. Large Cell CarcinomaLarge Cell Carcinoma
10% to 20% of all lung cancers.
Most are peripheral, poorly marginated masses (>7
cm) in size.
Typically rapid growth
cavitation is uncommon.
Hilar and mediastinal adenopathy occurs in up to one
third of patients at presentation.
Early extrathoracic metastases are common
31. A, PA chest radiograph shows a
large lobular mass in the right
upper lobe. Cavitation is present,
with an air-fluid level in the upper
aspect of the mass.
B, CT scan shows a well-
circumscribed mass with eccentric
cavitation and thick walls. Note the
nonenlarged paratracheal and left
lower paratracheal lymph nodes
(arrowheads).
Large cell lung cancer manifesting as a large cavitary mass
33. SMALL CELL LUNG CARCINOMASMALL CELL LUNG CARCINOMA
15% to 20% of all lung cancers.
1° tumor is typically small & central in location.
Associated with marked hilar and mediastinal adenopathy
Distant metastases to liver, bone marrow, adrenals, and
brain
Pleural effusions occur in 5% to 40% of patients.
5% of SCLCs manifest as small, peripheral, solitary
pulmonary nodules without intrathoracic adenopathy,
disseminated extrathoracic disease, or pleural effusions
34. Small cell lung cancer with
intrathoracic adenopathy
A: PA chest radiograph shows
marked right hilar adenopathy
B: CT scans shows marked right
hilar and subcarinal adenopathy
C: CT scans shows a small primary
malignancy (arrow) in rt. upper lobe
35. A, PA chest radiograph shows
-a large, poorly marginated right mass
-multicompartmental mediastinal
adenopathy
-obstructive consolidation &
atelectasis of the right lung
B, CT scan confirms
-marked hilar and mediastinal
adenopathy
-marked narrowing of the bronchus
intermedius (asterisk).
-consolidative and atelectatic
opacities distal to the large right hilar
mass
-small right effusion
Small cell lung cancer manifesting as extensive hilar and
mediastinal adenopathy
36. Clinical ManifestationsClinical Manifestations
Most patients in fifth or sixth decade and symptomatic at presentation.
Variable symptoms depending upon :-
- Local effects of the primary mass,
- Presence of regional or distant metastases,
- Coexistence of paraneoplastic syndromes.
Central endobronchial carcinomas: manifest as fever, dyspnea, hemoptysis,
and cough.
Cough with copious amounts of watery sputum (bronchorrhea) typically in
patients with BAC and extensive parenchymal disease (rare).
Symptoms as a result of local growth and invasion of adjacent structures:
- Chest pain (peribronchial nerve involvement);
- vocal cord paralysis and hoarseness (recurrent laryngeal nerve involvement)
- dyspnea due to diaphragmatic paralysis (phrenic nerve involvement)
- Horner's syndrome — ptosis, mycosis, anhidrosis (sympathetic chain and
stellate ganglion involvement by superior sulcus tumors)
- Facial swelling, headaches, enlarged collateral chest wall vessels (superior vena
cava obstruction)
- Dysphagia (esophageal invasion)
37. Non–small cell lung cancer in a 61-year-old woman presenting
with
hoarseness caused by involvement of the recurrent laryngeal nerve
A, PA chest radiograph shows a left
perihilar mass (arrow).
[Note a small effusion and pneumothorax
following transthoracic needle aspiration
biopsy (arrowheads)]
B, CT scan reveals mediastinal
invasion, with extension of the
mass into the aortopulmonary
window. Arrows show the mass in
the recurrent laryngeal nerve.
(Note the small pleural effusion)
38. PA chest radiograph shows a large lobular mass in the left lower lobe and
elevation of the left hemidiaphragm
Small cell lung cancer in a 50-year-old woman with
diaphragmatic paralysis resulting from phrenic nerve
involvement.
39. Non–small cell lung cancer in a 54-year-old man with a superior
sulcus (Pancoast) tumor and a 2-month history of neck pain
B, CT scan confirms the left
superior sulcus tumor
and destruction of the left
first rib
A, PA chest radiograph shows a left
apical mass, with destruction of
the first rib (arrowheads)
40. Symptoms related to extrathoracic metastases are mostly bone pain
or central nervous system (CNS) abnormalities.
Paraneoplastic syndromes occur in 10% to 20% of lung cancer patients
and are usually associated with SCLC.
Antidiuretic and adrenocorticotropic hormones are the more
frequently excreted hormones resulting in hyponatremia and in
Cushing's syndrome respectively.
Other hormones that may be elevated are calcitonin, growth hormone,
human chorionic gonadotropin, and, rarely, prolactin and serotonin.
Neurologic paraneoplastic syndromes (Lambert-Eaton myasthenic
syndrome, paraneoplastic cerebellar degeneration, paraneoplastic
encephalomyelitis, paraneoplastic sensory neuropathy) are rare and are
usually associated with SCLC.
The neurologic symptoms typically precede the diagnosis of lung
cancer by up to 2 years & progress rapidly.
Miscellaneous paraneoplastic syndromes associated with lung cancer
include acanthosis nigricans, dermatomyositis, disseminated
intravascular coagulation, and hypertrophic pulmonary
osteoarthropathy (most common, upto 17%).
41. Non–small cell lung cancer in an asymptomatic 64-year-old woman
A, CT scan shows a large right upper lobe mass
B, Technetium 99m–labeled methylene diphosphonate
bone scintigram shows linear areas of increased
radiotracer uptake in the femurs and tibias. This
appearance is characteristic of hypertrophic
pulmonary osteoarthropathy.
42. DiagnosisDiagnosis
Because most lung cancer have advanced disease at presentation, diagnosis is
usually not difficult.
Nevertheless, 20% to 30% of patients with lung cancer present with a
solitary pulmonary nodule that may be difficult to differentiate from a benign
nodule.
Certain morphologic and physiologic features, however, suggest a diagnosis
of lung cancer :-
Size:-Size:-
The larger the nodule, the more likely it is to be malignant.
Small size, does not exclude lung cancer (up to 42% of resected lung cancers
< 2 cm)
Margins:-Margins:-
Malignant typically have irregular or spiculated margins
Benign nodules typically have smooth margins.
(however, presence of one does not exclude the other)
43. Internal Morphology.Internal Morphology.
Fat ( 40 to 120 [HU]) and− − calcification, only features that are reliable in
distinguishing lung cancer from a benign nodule.
Calcification in malignant lesions is typically amorphous in appearance (found in
up to 14% of lung cancers ).
Calcification in benign lesions is diffuse, solid, central punctate, laminated,
or popcorn-like.
Likelihood of malignancy varies according to the degree of soft tissue attenuation.
- partially solid nodular opacities (63%),
- ground-glass opacities (18%)
- solid nodules (7%)
Cavitation occurs in benign nodules and lung cancer.
Malignant nodules : typically thick, irregular walls,
Benign nodules : smooth, thin walls.
GrowthGrowth.
Lung cancers typically double in volume between 30 and 400 days (avg. 240 days)
The measurement of serial volumes, rather than diameters, and the computer-
calculated doubling of volume of small nodules have been suggested as accurate and
potentially useful methods to assess growth
44. Non–small cell lung cancer manifesting as a calcified mass
CT scan shows a large right upper lobe mass with mediastinal invasion.
Scattered areas of amorphous calcification in the mass are typical of,
but not diagnostic for, malignancy
45. Low-Risk Populations (Little or No History of Smoking and NoLow-Risk Populations (Little or No History of Smoking and No
Other Risk Factors)Other Risk Factors)
Nodular size reassessment If stable If stable
≤4 mm not required
>4 mm but ≤6 mm CT at 12 months No further evaluation
>6 mm but ≤8 mm CT at 6 to 12 months CT at 18 to 24 months No further evaluation
>8 mm CT scans at 3, 9, and 24 months or further evaluation with contrast-
enhanced CT, CT PET, biopsy, or resection
High-Risk Populations (History of Smoking or Other Exposure orHigh-Risk Populations (History of Smoking or Other Exposure or
Risk Factor)Risk Factor)
Nodular size reassessment If stable If stable
≤4 mm CT at 12 months No further evaluation
>4 mm but ≤6 mm CT at 6 to 12 months CT at 18 to 24 months No further evaluation
>6 mm but ≤8 mm CT at 3 to 6 months CT at 9 to 12 months again 24 months
>8 mm CT scans at 3, 9, and 24 months or further evaluation with contrast-
enhanced CT, CT PET, biopsy, or resection
Fleischner Society Guidelines for the Evaluation ofFleischner Society Guidelines for the Evaluation of
Incidentally Discovered NodulesIncidentally Discovered Nodules
46. Blood SupplyBlood Supply
qualitatively and quantitatively different
In CECT - malignant nodules enhance > 20 HU,
benign nodules enhance <15 HU
A, NCCT scan shows a left lung
nodule with an attenuation value of
24 Hounsfield units (HU).
B, CECT scan shows nodule
enhancement of 70 HU and central
necrosis.
* Resection revealed non–small cell cancer
47. MetabolismMetabolism
Metabolism of glucose is typically increased in lung cancer cells
FDG (fluorodeoxyglucose ) uptake can be assessed visually on PET images by comparing the
activity of the lesion with that of the background.
FDG uptake is quantified by using standardized uptake value (SUV) or local metabolic rate of
glucose (Ki = influx constant).
SUV > 2.5 is considered indicative of malignancy.
The probability of malignancy is high when a solid nodule ≥ 1 cm shows increased FDG uptake
These nodules should be biopsied or resected and thus FDG PET can reduce the number of
benign nodules resected.
A, CT scan shows a spiculated nodule
in the right upper lobe. The irregular
margin suggests malignancy.
B, Axial fused CT PET image with FDG
shows increased uptake within the nodule
compared with the adjacent mediastinum.
These findings are suspicious for
malignancy.
* Transthoracic needle aspiration biopsy revealed adenocarcinoma
48. International Staging System for Lung CancerInternational Staging System for Lung Cancer
Primary Tumor (T)Primary Tumor (T)
TxTx Primary tumor cannot be assessed, or tumor proved by the presence of malignant cells in sputum or bronchial washings
but not visualized by imaging or bronchoscopy
T0T0 No evidence of primary tumor
TisTis Carcinoma in situ
T1T1 Tumor ≤3 cm in greatest dimension, surrounded by lung or visceral pleura, without bronchoscopic evidence of invasion
more proximal than the lobar bronchus[*]
(i.e., not in the main bronchus)
T2T2 Tumor with any of the following features of size or extent: >3 cm in greatest dimension; Involves main bronchus, ≥2 cm
distal to the carina; Invades the visceral pleura; Associated with atelectasis or obstructive pneumonitis that extends to
the hilar region but does not involve the entire lung
T3T3 Tumor of any size that directly invades any of the following: chest wall (including superior sulcus tumors), diaphragm,
mediastinal pleura, or parietal pericardium; or tumor in the main bronchus <2 cm distal to the carina, but without
involvement of the carina; or associated atelectasis or obstructive pneumonitis of the entire lung
T4T4 Tumor of any size that invades any of the following: mediastinum, heart, great vessels, trachea, esophagus, vertebral
body, or carina; or tumor with a malignant pleural or pericardial effusion[†]
or with satellite tumor nodule(s) within the
ipsilateral primary-tumor lobe of the lung
Regional Lymph Nodes (N)Regional Lymph Nodes (N)
NxNx Regional lymph nodes cannot be assessed
N0N0 No evidence of regional lymph node metastasis
N1N1 Metastasis to : ipsilateral peribronchial and/or ipsilateral hilar lymph nodes
: intrapulmonary nodes involved by direct extension of the primary tumor
N2N2 Metastasis to : ipsilateral mediastinal and/or subcarinal lymph node(s)
N3N3 Metastasis to : contralateral mediastinal or hilar lymph node(s)
: ipsilateral or contralateral scalene, or supraclavicular lymph node(s)
Distant Metastasis (M)Distant Metastasis (M)
MxMx Presence of distant metastasis cannot be assessed
M0M0 No distant metastasis
M1M1 Distant metastasis present[‡]
* Superficial tumor of any size limited to the bronchial wall, is also classified as T1.
† In a few patients, cytopathologic examinations of pleural/pericardial fluid show no tumor, is nonbloody and non-exudative. Then it should be
excluded as a staging element, and the patient's disease should be staged T1, T2, or T3.
‡ Separate metastatic tumor nodule(s) in the ipsilateral nonprimary-tumor lobe(s) of the lung are also classified M1.
49. Primary Tumor (T Status)Primary Tumor (T Status)
Imaging is performed to assess the degree of pleural, chest wall, and mediastinal
invasion.
CT: used for gross chest wall invasion (inaccurate in differentiating between
anatomic contiguity and subtle invasion)
Findings suggestive of chest wall invasion include :
• Tumor-pleura contact extending over > 3 cm
• Obtuse angle at the tumor-pleura interface
• Thickening of the pleura or increased attenuation of the extrapleural fat
adjacent to the tumor
A: PA chest radiograph shows a large
cavitary right lower lobe lung mass
(arrows) and destruction of the posterior
aspect of the right seventh rib (arrowheads).
B: CT scan confirms the cavitary mass (M)
and destruction of the adjacent rib (asterisk).
Note the extension of the mass into the
chest wall (arrowheads)
50. Although MRI offers superior soft tissue contrast resolution, its sensitivity
and specificity in identifying chest wall invasion are similar to that of CT.
MRI is particularly helpful in evaluating superior sulcus (Pancoast) tumors and to
assess invasion of the brachial plexus, subclavian vessels, and vertebral bodies.
A, CT scan shows a large, well-
circumscribed peripheral lung mass
with invasion of the chest wall
B, Coronal fast-spin echo MRI
shows the mass abutting the chest
wall and the surrounding ribs
(asterisk) and extending through
the intercostal space into the soft
tissues of the chest wall (arrow).
Coronal T1-weighted image shows a mass (M) in the
apex of the right hemithorax, with invasion into
the neck. The mass surrounds the subclavian
artery (asterisk) and the brachial plexus. (R, first
51. Findings suggestive of subtle mediastinal invasion include :
• Tumor-mediastinum contact extending over > 3 cm
• Obliteration of the fat plane between the mediastinum and the tumor
• Tumor contacting > 90° of the aortic circumference
CT scan shows a large left upper lobe mass,
with invasion of the anterior mediastinum.
Broad abutment and loss of the soft tissue
plane between the mass and the transverse
aorta suggest vascular invasion
Double inversion recovery, contrast-enhanced,
single breath-hold coronal MRI shows an
enhancing right upper lobe mass (M) that
extends via the right superior pulmonary vein
into the left atrium (LA).
52. Primary lesions associated with malignant pleural effusions or pleural
metastases are classified as T4 lesions.
Up to 33% of NSCLC show pleural metastases at presentation.
Pleural thickening and nodularity on CT scans suggest metastatic pleural
disease.
Contrast-enhanced CT scan shows a large right pleural effusion and enhancing nodular
pleural metastases (arrowheads). Arrow indicates compressive atelectasis of the right lower
lobe and a metastatic left rib lesion
53. To enable a consistent and standardized description of N status, nodal
stations are defined by the American Thoracic Society in relation to
anatomic structures or boundaries that can be identified before and during
thoracotomy.
The IASLC has proposed six zones within the current N1 and N2 patient
subsets for further evaluation.
The zones consist of
- peripheral (stations 12, 13, 14)
- hilar (stations 10, 11)
&
- upper mediastinal (stations 1, 2, 3, 4)
- lower mediastinal (stations 8, 9)
- aortopulmonary (stations 5, 6)
- subcarinal (station 7)
Regional Lymph Nodes (N Status)Regional Lymph Nodes (N Status)
N1
N2
55. NSCLC commonly show extrathoracic metastases to the adrenal glands, liver, brain,
bones, and lymph nodes at presentation.
FDG PET - higher sensitivity and specificity than CT
Adrenal glands metastases : Common, detected in up to 20% of patients at presentation.
Features favouring malignancy :
• Size > 3 cm
• Poorly defined margins
• Irregularly enhancing rim
• Invasion of adjacent structures
• High signal intensity on T2
Metastatic Disease (M Status)Metastatic Disease (M Status)
A: CT scan shows a nodule in the left lower lobe.
There is no hilar or mediastinal adenopathy
B: CT scan of the abdomen reveals a left adrenal
mass (arrow). Biopsy confirmed metastasis
56. CNS metastases –
Detected in up to 18 % of patients at presentation.
Routine CT of the brain suggested in the initial staging evaluation of all patients with
NSCLC
Not recommended as : CNS metastases usually associated with neurologic signs and
symptoms & not cost-effective.
ASCO recommends brain CT or MRI for asymptomatic patients in stage III being
considered for aggressive local therapy (viz. thoracic surgery or radiation).
A: CT scan shows a 3.5 cm
spiculated left upper lobe mass.
B: Axial contrast-enhanced cranial MR image shows
an enhancing metastasis in the cerebellum (arrow).
57. Skeletal metastases :
Usually symptomatic or have laboratory abnormalities indicating bone
metastases.
Bone radiographs, MRI, and bone scintigraphy : performed to evaluate h/o focal
bone pain or elevated alkaline phosphatase.
FDG PET help in detecting occult osseous metastases.
A: PA chest radiograph
shows a right upper lobe
mass. There is a small right
pleural effusion.
B: CT scan reveals a small right
adrenal mass (arrow) and confirms a
small right pleural effusion.
C, Whole-body FDG PET shows increased uptake in the primary lung mass (small arrow) and in the
adrenal metastasis (arrowhead). Focal areas of increased uptake in the upper aspect of the left
hemithorax and pelvis (large arrows) were unsuspected bone metastases.
58. Stage Grouping: Tumor-Node-MetastasesStage Grouping: Tumor-Node-Metastases
(TNM) Subsets(TNM) Subsets
Stage
TNM Subset
T N M
IA T1 N0 M0
IB T2 N0 M0
IIA
T1 N1 M0
T2 N1 M0
IIB T3 N0 M0
IIIA
T1 N2 M0
T2 N2 M0
T3 N1 M0
T3 N2 M0
IIIB
T4 N0 M0
T4 N1 M0
T4 N2 M0
T1 N3 M0
T2 N3 M0
T3 N3 M0
T4 N3 M0
IV Any T Any N M1
59. Staging of Small Cell Lung CarcinomaStaging of Small Cell Lung Carcinoma
SCLC staged according to Veterans Administration Lung Cancer Study Group (VALCG)
recommendations :
i)i) Limited disease (LD)Limited disease (LD) :: confined to a hemithorax and the regional lymph nodes.
Unlike TNM classification for NSCLC, metastases to both ipsilateral & contralateral
supraclavicular and mediastinal lymph nodes are considered local disease.
ii)ii) Extensive disease (ED)Extensive disease (ED) :: includes noncontiguous metastases to the contralateral lung
and distant metastases.
Most patients present with ED.
Common sites of metastasis: liver (30%), bone (30%), bone marrow (17 to 34%), brain (10
to 27%), and retroperitoneal lymph nodes (11%).
Evaluation includes bone marrow aspiration, bone scintigraphy and MRI of the brain and
abdomen.
A: PA chest radiograph shows a lobular
3-cm right upper lobe nodule (arrow)
and hilar adenopathy (arrowhead).
B: CT scan shows a left
adrenal metastasis
(arrow).
C, Axial contrast-enhanced cranial MR
image shows an enhancing cerebellar
metastasis (arrow).
61. Contains carcinomatous and sarcomatous components.
Includes pulmonary blastoma, carcinosarcoma, and carcinomas with spindle
or giant cells.
Rare - 0.3% to 1%
Most patients are men, mean age at presentation :65 yrs (range, 44 to 78 yrs).
Usually localized at presentation, distant metastases occur frequently, prognosis is
poor.
Mostly present with cough, dyspnea, hemoptysis, chest pain, or weight loss.
Radiologically manifest as either
- large peripheral masses or
- polypoid endobronchial lesions with atelectasis or
- postobstructive pneumonia.
Calcification and cavitation are uncommon
Necrosis and hemorrhage can manifest as heterogeneous attenuation on CT.
Hilar or mediastinal adenopathy is uncommon.
Pleural effusion can occur as a result of local invasion.
Metastases involve sites similar to those associated with lung cancer: lungs, liver,
bones, adrenals, brain
Sarcomatoid CarcinomaSarcomatoid Carcinoma
62. Rare, 0.25% to 0.5% of primary lung tumors.
Named so for histologic resemblance to fetal lung tissue.
Thought to arise from primitive pluripotential stem cells and may represent a
variant of carcinosarcoma.
Mainly in adults, peak incidence between 40 and 60 yrs of age.
Often symptomatic at presentation; cough, hemoptysis, and chest pain are
frequent manifestations.
Pediatric patients typically present with fever and respiratory distress.
Aggressive with poor prognosis owing to frequent relapses and metastases.
Radiologically: Typically manifest as
- large (2.5 to 26 cm),
- well-marginated masses
- located peripherally in the lung
Multiple masses, cavitation, and calcification are rare.
Local invasion : mediastinum (8%) and pleura (25%)
Metastases to hilar and mediastinal lymph nodes (30%)
Extrathoracic metastases common with distribution similar to that of lung cancer
Pulmonary BlastomaPulmonary Blastoma
63. Pulmonary blastoma manifesting as a large pulmonary
mass
A: PA chest radiograph shows complete
homogeneous opacification of the left
hemithorax and displacement of the
mediastinum to the right.
B: CT scan reveals a large lung mass and
shows heterogeneous attenuation
consistent with necrosis. There is
subcarinal adenopathy due to
metastatic disease (asterisk). Note the
complete compressive atelectasis of the
left lung.
65. Low-grade malignancies, constitute 1% to 2% of primary lung tumors.
Classified histologically depending on the degree of cellular atypia as :
i) Typical (80% to 90%) or ii) Atypical (10% to 20%)
TypicalTypical : equal frequency in men and women;
- Mean age at diagnosis is 35 to 50 years.
- Usually arise in lobar, segmental, or proximal subsegmental bronchi
- generally measure 1 to 4 cm
- Rarely metastasize to regional nodes or beyond the thorax
AtypicalAtypical : slightly older age (mean, 53 to 60 years),
- Often larger
- Occur more frequently in the peripheral aspect of the lungs.
-More aggressive, frequent metastasis to regional nodes, lung, liver &
bone. N status most important prognostic factor.
Clinical manifestations depend on histologic type and location
Peripheral tumors usually asymptomatic, whereas central one manifest as
cough, hemoptysis, or recurrent infection.
Paraneoplastic manifestations, viz. carcinoid syndrome and Cushing's syndrome,
are rare and more common with atypical carcinoid tumors.
Carcinoid TumorCarcinoid Tumor
66. Radiologically : carcinoid tumors manifest most commonly as central
endobronchial masses, with or without atelectasis or consolidation.
A peripheral, well marginated pulmonary
nodule is a less common manifestation.
A: PA chest radiograph shows complete
atelectasis of the right lower lobe
(arrowheads), with compensatory
hyperinflation of the left lung. Note the
displacement of the anterior junction line
(arrows).
B: CT scan confirms atelectasis of the right
lower lobe and reveals an endobronchial
mass (M), with marked narrowing of the
bronchus intermedius (arrow)
CT scan shows a small, well-circumscribed nodule
in the left lower lobe (arrow).
67. The tumors are usually < 3 cm, although occasionally they may be as large as 10
cm in diameter.
Calcification is detected by CT in approximately 25% of carcinoid tumors
Hilar and mediastinal adenopathy and extrathoracic metastases are
uncommon at presentation in patients with typical carcinoid tumors; they occur
CT scan shows a large
endobronchial mass with
dense punctate calcification
69. Formerly categorized as bronchial adenoma
A rare tracheobronchial tumor composed of distinct areas of
squamoid cells, mucus-secreting cells, and cells of
intermediate type.
More common in adults, peak incidence between 35 and 45 yrs.
Typically occur in the main or lobar bronchi
Rarely may be located in the trachea and periphery of the lung.
Slow-growing, low-grade neoplasms with a benign clinical course.
Occasionally exhibit aggressive local behavior,
Metastases are uncommon.
Radiologically the tumor manifests:
- Usually as a central endobronchial mass
- less commonly, as a polypoid intraluminal tracheal mass
or a peripheral lung nodule or mass
Mucoepidermoid CarcinomaMucoepidermoid Carcinoma
SALIVARY GLAND TUMORSSALIVARY GLAND TUMORS
71. Formerly categorized as bronchial adenoma.
Uncommon 1° tumor of the lung, occurs mainly in the trachea &
main bronchi, only 10%-15% found in peripheral lung field.
Equal frequency in men and women; the mean age at diagnosis is 45
to 51 years
Adenoid Cystic Carcinoma (Cylindroma)Adenoid Cystic Carcinoma (Cylindroma)
They typically exhibit slow,
progressive growth.
Metastases to regional lymph
nodes, lung, bone, liver, and brain
occur late.
Radiologically : usually manifests
as an lobulated or an polypoidal
endotracheal or endobronchial mass
encroaching the airway lumen.
Masses can be circumferential
and may manifest as diffuse stenosis.
A less common manifestation is a
peripheral lung nodule or mass.
CT scan shows a circumferential
soft tissue tracheal mass (T) and
narrowing of the trachea
73. Most Primary lung sarcomas with a vascular origin eg. Angiosarcomas &
epithelioid hemangioendotheliomas, are lung metastases, and the
existence of primary pulmonary angiosarcoma are rare.
The Angiosarcomas usually occurs in young adults where as
Epithelioid hemangioendothelioma is typically seen in women
younger than 40 years.
Most patients are asymptomatic at presentation
Complaints include weight loss, dyspnea, chest pain, and cough.
Usual radiologic manifestation is multiple 1 to 2 cm bilateral
pulmonary nodules.
Calcification is rarely detected.
Hilar adenopathy and pleural effusions occur in 9% of patients.
Multiorgan involvement, most commonly the liver, occurs occasionally
and may represent metastatic disease or multicentric origin of the
tumor.
MESENCHYMAL TUMORSMESENCHYMAL TUMORS
((Primary Pulmonary Sarcomas)Primary Pulmonary Sarcomas)
74. Epithelioid hemangioendothelioma appearing as multiple
pulmonary nodules
A: PA chest radiograph shows
numerous small, bilateral pulmonary
nodules. Note the absence of hilar
and mediastinal adenopathy.
B: CT scan confirms the numerous
small, bilateral, well-circumscribed
nodules
C: CT scan of the abdomen reveals small,
bilateral, low-attenuation hepatic epithelioid
hemangioendotheliomas.
75. Primary lung sarcomas with a spindle cell origin are rare (< 0.5%)
Spindle cell sarcomas (malignant fibrous histiocytoma,
hemangiopericytoma, fibrosarcoma, leiomyosarcoma, synovial sarcoma)
are the most common primary pulmonary sarcomas.
Heterogeneous group of tumors with morphologic similarities to their
extrathoracic counterparts.
Diagnosis established after excluding metastasis and sarcoma-like primary lung
malignancies (sarcomatoid carcinomas).
Peak incidence between fifth and sixth decades.
Usually slow growing with late metastases, prognosis generally better than lung
cancer.
Radiologically: - Commonly located peripherally
- Lesions range in size from 0.6 to 25 cm
- Sharply marginated and occasionally calcified
- Cavitation is uncommon,
- heterogeneous attenuation from necrosis on CT
-Pathognomonic hypervascularity are seldom seen on CT or
MRI scans of primary pulmonary hemangiopericytomas
76. Malignant fibrous histiocytoma manifesting as a large
lung mass.
A: PA chest radiograph shows a left
upper lobe mass
B: CT scan shows a large lobular mass and
narrowing of the left main pulmonary artery
(arrowheads).
77. Synovial carcinoma of left lung manifesting as a large
mass
A, CT scan shows a large
mass in the left lower lobe,
with a small focal
calcification (arrow). A small
pleural effusion can also be
seen
B and C, Coronal T1-weighted (B) and fast-spin echo (C)
images show a large heterogeneous mass (M) abutting
the diaphragm, without signs of invasion. There is a small
pleural effusion (P). L, liver
78. Hemangiopericytoma appearing as a large hypervascular
mass
A, Contrast-enhanced CT scan shows
a large right lower lobe mass. Large
vessels can be seen within the mass
B and C, Axial T1-weighted (B) and fast-spin echo (C) images show a
heterogeneous mass in the right hemithorax. Flow voids can be seen
within the intratumoral vessels.
80. Primary pulmonary lymphomas account for <1% of all lymphomas.
Diagnosis made if lymphoid proliferation is monoclonal and there are no sites
of extrathoracic lymphoma at presentation or for at least 3 months after
diagnosis.
1° pulmonary lymphomas encompass non-Hodgkin‘s & Hodgkin's lymphoma,
and lymphoproliferative disorders associated with immunodeficiency states.
Most primary extranodal lymphomas arise from mucosa-associated
lymphoid tissue (MALT)
Typically infiltrate the bronchiolar mucosal epithelium, forming
lymphoepithelial lesions.
Primary pulmonary lymphomas tend to remain localized to the lung
Recurrence after treatment - up to 50% (often at extrapulmonary sites)
Radiologic manifestations :
- a solitary nodule or mass - multiple nodules or masses,
- focal or multifocal consolidation - reticulonodular opacities
- atelectasis - Hilar adenopathy (rare)
- pleural effusions (in 7% to 25% )
LYMPHOPROLIFERATIVE DISORDERS:LYMPHOPROLIFERATIVE DISORDERS:
(Primary Lymphomas)(Primary Lymphomas)
81. Primary pulmonary lymphoma manifesting as bilateral
pulmonary opacities
A and B, CT scans show focal, poorly marginated nodular opacities in both lungs. Air-
bronchograms within opacities are suggestive of the diagnosis.
83. Constitute 0.25% of all primary lung tumors
Most common benign tumor of the lung
Term hamartoma initially used to describe lesions with abnormal composition or
disorganized arrangement of normal lung tissue.
Now considered true neoplasms containing a mixture of epithelial and
mesenchymal tissues.
Typically occur in patients >30 years (peak incidence in the sixth decade)
Most patients are asymptomatic
Symptoms are typically present with central endobronchial lesions and
include hemoptysis, recurrent pneumonia, and dyspnea.
Hamartomas are typically solitary, well-marginated, slightly lobular nodules
or masses < 4 cm
Most are located peripherally within the lung.
Endobronchial hamartomas are less common (< 20%)
Calcification < 5%
“PopcornPopcorn” calcification pathognomonic of hamartomas.
Fat occurs in up to 50% of cases and is a diagnostic feature
Cavitation and multiple pulmonary hamartomas are rare
HAMARTOMASHAMARTOMAS
84. Hamartoma manifesting as a large mass
Hamartoma appearing as a solitary pulmonary nodule
CT scan shows a left upper lobe nodule
(arrow) anterior to the left pulmonary artery.
The diagnosis is suggested by small areas
of fat (attenuation, 41 Hounsfield units)−
within the nodule
CT scan shows a right lower lobe mass that has
focal calcified regions as well as focal regions
of low attenuation ( 60 Hounsfield units),−
consistent with fat.
The diagnosis is suggested by small areas
of fat within the mass
86. Formerly called granular cell myeloblastomas
Uncommon benign mesenchymal neoplasms, thought to arise from
Schwann cells
Usually present as a small solitary skin or submucosal nodule.
Pulmonary granular cell tumors – rare (6 - 10% of all granular cell tumors)
Patients are usually adults (peak incidence, 30 to 50 years)
Higher incidence in African Americans.
Mostly manifest as small (0.3 to 6.5 cm in diameter), central
endobronchial masses.
Multiple lesions, typically in the larger bronchi, are found in up to 25% of
cases.
Common radiologic findings include atelectasis and obstructive
pneumonia
Slow-growing, solitary pulmonary nodules or masses occur in 12% of
cases
GRANULAR CELL TUMORGRANULAR CELL TUMOR
88. Formerly called pneumocytoma or papillary pneumocytoma
A benign tumor consisting of thin-walled vessels and connective
tissue.
Originally thought to represent a vascular tumor, now believed to arise
from primitive respiratory epithelium.
Most patients are asymptomatic women between 30 and 50 years of
age.
However, cough and hemoptysis can occur in few.
Radiologically, usually manifest as peripheral, well-marginated,
solitary pulmonary nodule or mass 0.4 to 8 cm in diameter (average,
3 cm).
Multiple pulmonary nodules and calcification are rare.
Marked contrast enhancement is typical on CT, and tumors are
typically heterogeneous in attenuation due to the angiomatous,
solid and sclerotic, and cystic composition of the tumor.
MRI appearance is variable showing both homogeneous and
heterogeneous signal intensity.However, useful in diagnosis when regions
of different signal intensities are present in the tumor.
SCLEROSING HEMANGIOMASCLEROSING HEMANGIOMA
90. A rare neoplasm of the lung.
Most patients asymptomatic, between 50 and 60 years of age
Almost all behave in a benign nature, although extrathoracic metastases have been
reported.
Manifest radiologically as well-marginated, solitary pulmonary nodules < 3
cm in diameter.
CLEAR CELL TUMORCLEAR CELL TUMOR
CT scan shows a well-circumscribed left upper lobe nodule with heterogeneous
enhancement
Changes proposed by the IASLC, based on differences in survival:
• T1 subclassified as T1a (&lt;2 cm) or T1b (&gt;2 to &lt;3 cm) • T2 subclassified as T2a (&gt;3 to &lt;5 cm) or T2b (&gt;5 to &lt;7 cm) • T2 tumors greater than 7 cm subclassified as T3 • Reclassify T4 tumors by additional nodule(s) in the lung (primary lobe) as T3 • Reclassify M1 by additional nodule(s) in the ipsilateral lung (different lobe) as T4 • Reclassify pleural dissemination (malignant pleural effusions, pleural nodules) as M1
International Association for the Study of Lung Cancer (IASLC)