DEPARTMENT OF PHYSIOTHERAPY.
ASSIGNMENT TITLE:
Profound Discussion On Cancer.
SUBMITTED BY:
AYOUB ZUBEIR.
Physiotherapy Student.
SUBMITTED TO:
Chief. ALOYCE BWANA.
MLOGANZILA NATIONAL HOSPITAL.
DATE OF SUBMISSION:
Saturday, 14th September 2024.
OVERVIEW OF LUNG CANCER
Lung carcinoma is the leading cause of cancer-related death in men and
women worldwide. About 85% of cases are related to cigarette smoking.
Symptoms can include cough, chest discomfort or pain, weight loss, and, less
commonly, hemoptysis; however, many patients present with metastatic
disease with or without any clinical symptoms. The diagnosis is typically
made by chest x-ray or CT and confirmed by biopsy. Depending on the stage
of the disease, treatment includes surgery, chemotherapy, radiation therapy,
or a combination. For the past several decades, the prognosis for a lung
cancer patient was poor, with only 15% of patients surviving 5 years from
the time of diagnosis. For patients with stage IV (metastatic) disease, the 5-
year overall survival rate was 1%. However, outcomes have improved
because of the identification of certain mutations that can be targeted for
therapy, and current 5-year survival rates are 41% (23% for women and 16%
for men).
Tumors
A variety of benign and malignant tumors may arise in the lung, but 90% to
95% are carcinomas, about 5% are bronchial carcinoids, and 2% to 5% are
mesenchymal and other miscellaneous neoplasms.
CARCINOMAS
Lung cancer is currently the most frequently diagnosed major cancer in the
world and the most common cause of cancer mortality worldwide. This is
largely due to the carcinogenic effects of cigarette smoke. Over the coming
decades, changes in smoking habits will greatly influence lung cancer
incidence and mortality as well as the prevalence of various histologic types
of lung cancer.
The number of new cases of lung cancer occurring in 2008 in the United
States is estimated to be 215,020 (note that in 1950 it was 18,000),
accounting for about 15% of cancer diagnoses and 29% of cancer-related
deaths. The annual number of deaths from lung cancer in the United States
is estimated to be 161,840 in 2008.139 Since the early 1990s lung cancer
incidence and mortality rates have been decreasing in men, most likely from
the decreased smoking rates over the past 30 years. However, decreases in
smoking patterns among women lag behind those of men. Since 1987 more
women have died each year of lung cancer than of breast cancer, which for
over 40 years had been the major cause of cancer death in women. Cancer
of the lung occurs most often between ages 40 and 70 years, with a peak
incidence in the 50s or 60s. Only 2% of all cases appear before the age of 40.
The outlook for individuals diagnosed with lung cancer is dismal. The 1-year
survival rate has increased from 34% in 1975 to 41% in 2007, largely
because of improvements in surgical techniques. However, the 5-year rate
for all stages combined is only 16%.
Pathogenesis.
Most carcinomas of the lung, similar to cancer at other sites, arise by a
stepwise accumulation of genetic abnormalities that transform benign
bronchial epithelium to neoplastic tissue. Unlike many other cancers,
however, the major environmental insult that inflicts genetic damage is
known. We begin our discussion with the well-known lung carcinogen—
cigarette smoke.
Etiology
Tobacco Smoking. The evidence provided by statistical and clinical
observations establishing a positive relationship between tobacco smoking
and lung cancer is overwhelming. Experimental data have also been
pursued, but this approach is limited by species differences.
Statistical evidence is most compelling: 87% of lung carcinomas occur in
active smokers or those who stopped recently.
Clinical evidence is obtained largely through observations of histologic
changes in the lining epithelium of the respiratory tract in habitual smokers.
Industrial Hazards. Certain industrial exposures increase the risk of
developing lung cancer. High-dose ionizing radiation is carcinogenic. There
was an increased incidence of lung cancer among survivors of the Hiroshima
and Nagasaki atomic bomb blasts. Uranium is weakly radioactive, but lung
cancer rates among nonsmoking uranium miners are four times higher than
those in the general population, and among smoking miners they are about
10 times higher.
The risk of lung cancer is increased with asbestos. Lung cancer is the
most frequent malignancy in individuals exposed to asbestos, particularly
when coupled with smoking. Asbestos workers who do not smoke have a five
times greater risk of developing lung cancer than do nonsmoking control
sub-jects, and those who smoke have a 50 to 90 times greater risk. The
latent period before the development of lung cancer is 10 to 30 years.
Air Pollution. Atmospheric pollutants may play some role in the increased
incidence of lung carcinoma today. Attention has been drawn to the potential
problem of indoor air pollution, especially by radon. Radon is a ubiquitous
radioactive gas that has been linked epidemiologically to increased lung
cancer in miners exposed to relatively high concentrations. The pathogenic
mechanism is believed to be inhalation and bronchial deposition of
radioactive decay products that become attached to environmental aerosols.
These data have generated concern that low-level indoor exposure (e.g., in
homes in areas of high radon in soil) could also lead to increased incidence of
lung tumors; some attribute the bulk of lung cancers in nonsmokers to this
insidious carcinogen.
Molecular Genetics. Ultimately, the exposures cited previously are thought
to act by causing genetic alterations in lung cells, which accumulate and
eventually lead to the neoplastic phenotype. It has been estimated that 10 to
20 genetic mutations have occurred by the time the tumor is clinically
apparent.
Precursor Lesions. Three types of precursor epithelial lesions are
recognized: (1) squamous dysplasia and carcinoma in situ, (2) atypical
adenomatous hyperplasia, and (3) diffuse idiopathic pulmonary
neuroendocrine cell hyperplasia. It should be noted that the term precursor
does not imply that progression to cancer will occur in all cases. Currently it
is not possible to distinguish between precursor lesions that progress and
those that remain localized or regress.
Classification.
Tumor classification is important for consistency in patient treatment and
because it provides a basis for epidemiologic and biologic studies. The most
recent classification of the World Health Organization has gained wide
acceptance (Table 15–10). Several histologic variants of each type of lung
cancer are described; however, their clinical significance is still
undetermined, except as mentioned below. The relative proportions of the
major categories are:
Adenocarcinoma (males 37%, females 47%)
Squamous cell carcinoma (males 32%, females 25%)
Small cell carcinoma (males 14%, females 18%)
Large cell carcinoma (males 18%, females 10%).
Robbins and Cotran Pathologic Basis of Disease, Chapter 15 (THE
LUNG), page 723, Table 15-10.
The incidence of adenocarcinoma has increased significantly in the last two
decades; it is now the most common form of lung cancer in women and, in
many studies, men as well. The basis for this change is unclear.
A possible factor is the increase in women smokers, but this only highlights
our lack of knowledge about why women tend to develop more
adenocarcinomas. One interesting postulate is that changes in cigarette type
(filter tips, lower tar and nicotine) have caused smokers to inhale more
deeply and thereby expose more peripheral airways and cells (with a
predilection to adenocarcinoma) to carcinogens. There may be mixtures of
histologic patterns, even in the same cancer. Thus, combined types of
squamous cell carcinoma and adenocarcinoma or of small-cell and squamous
cell carcinoma occur in about 10% of patients. For common clinical use,
however, the various histologic types of lung cancer can be clustered into
two groups on the basis of likelihood of metastases and response to available
therapies: small cell carcinomas (almost always metastatic, high initial
response to chemotherapy) versus non-small cell carcinomas (less often
metastatic, less responsive). The strongest relationship to smoking is with
squamous cell and small cell carcinoma.
Staging. A uniform TNM system for staging cancer according to its anatomic
extent at the time of diagnosis is extremely useful, chiefly y for comparing
treatment results from different centers (Table 15–11).
Clinical Course. Lung cancer is one of the most insidious and aggressive
neoplasms in the realm of oncology. In the usual case it is discovered in
patients in their 50s whose symptoms are of several months’ duration.
The major presenting complaints are:-
Cough (75%).
weight loss (40%).
Chest pain (40%).
Dyspnea (20%).
Some of the more common local manifestations of lung cancer and their
pathologic bases are listed in Table 15–12. Not infrequently the tumor is
discovered by its secondary spread during the course of investigation of an
apparent primary neoplasm elsewhere. Bronchioloalveolar carcinomas, by
definition, are noninvasive tumors and do not metastasize; unless resected,
they kill by suffocation.
Robbins and Cotran Pathologic Basis of Disease, Chapter 15 (THE
LUNG), page 728, Table15-11.
Robbins and Cotran Pathologic Basis of Disease, Chapter 15 (THE
LUNG), page 728, Table15-12.
Paraneoplastic Syndromes. Lung carcinoma can be associated with
several paraneoplastic syndromes, some of which may antedate the
development of a detectable pulmonary lesion. The hormones or hormone-
like factors elaborated include:
Antidiuretic hormone (ADH), inducing hyponatremia due to
inappropriate ADH secretion
Adrenocorticotropic hormone (ACTH), producing Cushing syndrome.
Parathormone, parathyroid hormone-related peptide, prostaglandin E,
and some cytokines, all implicated in the hypercalcemia often seen
with lung cancer.
Calcitonin, causing hypocalcemia
Gonadotropins, causing gynecomastia.
Serotonin and bradykinin, associated with the carcinoid syndrome.
The incidence of clinically significant syndromes related to these factors
ranges from 1% to 10% of all lung cancer patients, although a much higher
proportion of patients show elevated serum levels of these (and other)
peptide hormones. Any one of the histologic types of tumors may
occasionally produce any one of the hormones, but tumors that produce
ACTH and ADH are predominantly small cell carcinomas, whereas those that
produce hypercalcemia are mostly squamous cell tumors. The carcinoid
syndrome is more common with carcinoid tumors, described later, and is
only rarely associated with small cell carcinoma. However, small cell
carcinoma occurs much more commonly; therefore, one is much more likely
to encounter carcinoid syndrome in these patients.
Other systemic manifestations of lung carcinoma include the Lambert-
Eaton myasthenic syndrome, in which muscle weakness is caused by auto-
antibodies (possibly elicited by tumor ionic channels) directed to the
neuronal calcium channel; peripheral neuropathy, usually purely sensory;
dermatologic abnormalities, including acanthosis nigricans; hematologic
abnormalities, such as leukemoid reactions; and finally, a peculiar
abnormality of connective tissue called hypertrophic pulmonary
osteoarthropathy, associated with clubbing of the fingers.
Apical lung cancers in the superior pulmonary sulcus tend to invade the
neural structures around the trachea, including the cervical sympathetic
plexus, and produce a group of clinical findings that includes severe pain in
the distribution of the ulnar nerve and Horner syndrome (enophthalmos,
ptosis, miosis, and anhidrosis) on the same side as the lesion. Such tumors
are also referred to as Pancoast tumors.
NEUROENDOCRINE PROLIFERATIONS AND TUMORS
The normal lung contains neuroendocrine cells within the epithelium as
single cells or as clusters, the neuroepithelial bodies. While virtually all
pulmonary neuroendocrine cell hyperplasia’s are secondary to airway fi
brosis and/or inflammation, a rare disorder called diffuse idiopathic
pulmonary neuroendocrine cell hyperplasia seems to be a precursor to the
development of multiple tumorlets and typical or atypical carcinoids.
Neoplasms of neuroendocrine cells in the lung include benign tumorlets,
small, inconsequential, hyperplastic nests of neuroendocrine cells seen in
areas of scarring or chronic inflammation; carcinoids; and the (already
discussed) highly aggressive small cell carcinoma and large cell
neuroendocrine carcinoma of the lung. Neuroendocrine tumors are classified
separately, since there are significant differences between them in incidence,
clinical, epidemiologic, histologic, survival, and molecular characteristics. For
example, in contrast to small cell and large cell neuroendocrine carcinomas,
both typical and atypical carcinoids can occur in patients with multiple
endocrine neoplasia type 1.
Carcinoid Tumors. Carcinoid tumors represent 1% to 5% of all lung
tumors. Most patients with these tumors are younger than 40 years of age,
and the incidence is equal for both sexes. Approximately 20% to 40% of
patients are non-smokers. Carcinoid tumors are low-grade malignant
epithelial neoplasms that are sub classified into typical and atypical
carcinoids. Typical carcinoids have no p53 mutations or abnormalities of
BCL2 and BAX expression, while atypical carcinoids show these changes in
20% to 40% and 10% to 20% of tumors, respectively. Some carcinoids also
show loss of heterozygosity at 3p, 13q14 (RB1), 9p, and 5q22, which are
found in all neuroendocrine tumors with increasing frequency from typical to
atypical carcinoid to large cell neuroendocrine and small cell carcinoma.
Clinical Features. The clinical manifestations of bronchial carcinoids
emanate from their intraluminal growth, their capacity to metastasize, and
the ability of some of the lesions to elaborate vasoactive amines. Persistent
cough, hemoptysis, impairment of drainage of respiratory passages with
secondary infections, bronchiectasis, emphysema, and atelectasis are all by-
products of the intraluminal growth of these lesions.
MISCELLANEOUS TUMORS
Lesions of the complex category of benign and malignant mesenchymal
tumors, such as inflammatory myofibroblastic tumor, fibroma, fibro sarcoma,
lymphangioleiomyomatosis, leiomyoma, leiomyosarcoma, lipoma,
hemangioma, hemangiopericytoma, and chondroma, may occur but are rare.
Benign and malignant hematopoietic tumors, similar to those described in
other organs, may also affect the lung, either as isolated lesions or, more
commonly, as part of a generalized disorder. These include Langerhans cell
histiocytosis, non-Hodgkin and Hodgkin lymphomas, lymphomatoid
granulomatous, an unusual EBV-positive B cell lymphoma, and low-grade
marginal zone B-cell lymphoma of the mucosa-associated lymphoid tissue.
A lung hamartoma is a relatively common lesion that is usually discovered
as an incidental, rounded focus of radio-opacity (coin lesion) on a routine
chest fi lm. The majority of these tumors are peripheral, solitary, less than 3
to 4 cm in diameter, and well circumscribed. Pulmonary hamartoma consists
of nodules of connective tissue intersected by epithelial clefts. Cartilage is
the most common connective tissue, but there may also be cellular fibrous
tissue and fat. The epithelial clefts are lined by ciliated columnar epithelium
or nonciliated epithelium and probably represent entrapment of respiratory
epithelium.
The traditional term hamartoma is retained for this lesion, but several
features suggest that it is a neoplasm rather than a malformation, such as its
rarity in childhood, its increasing incidence with age, and the finding of
chromosomal aberrations involving either 6p21 or 12q14–q15, indicating a
clonal origin.
Inflammatory myofibroblastic tumor, though rare, is more common in
children, with an equal male-to-female ratio. Presenting symptoms include
fever, cough, chest pain, and hemoptysis. It may also be asymptomatic.
Imaging studies show a single (rarely multiple) round, well-defined, usually
peripheral mass with calcium deposits in about a quarter of cases. Grossly,
the lesion is firm, 3 to 10 cm in diameter, and grayish white. Microscopically,
there is proliferation of spindle-shaped fibroblasts and myofibroblasts,
lymphocytes, plasma cells, and peripheral fi brosis. The anaplastic lymphoma
kinase (ALK) gene, located on 2p23, has been implicated in the pathogenesis
of this tumor.
Tumors in the mediastinum either may arise in mediastinal structures or
may be metastatic from the lung or other organs. They may also invade or
compress the lungs. Table 15–13 lists the most common tumors in the
various compartments of the mediastinum. Specific tumor types are
discussed in appropriate sections of this book.
Robbins and Cotran Pathologic Basis of Disease, Chapter 15 (THE
LUNG), page 731, Table15-13.
METASTATIC TUMORS
The lung is the most common site of metastatic neoplasms. Both carcinomas
and sarcomas arising anywhere in the body may spread to the lungs via the
blood or lymphatics or by direct continuity. Growth of contiguous tumors into
the lungs occurs most often with esophageal carcinomas and mediastinal
lymphomas.
PLEURAL TUMORS
The pleura may be involved by primary or secondary tumors. Secondary
metastatic involvement is far more common than are primary tumors. The
most frequent metastatic malignancies arise from primary neoplasms of the
lung and breast. In addition to these cancers, malignancy from any organ of
the body may spread to the pleural spaces. Ovarian carcinomas, for
example, tend to cause widespread implants in both the abdominal and
thoracic cavities. In most metastatic involvements, a serous or
serosanguineous effusion follows that often contains neoplastic cells. For this
reason, careful cytologic examination of the sediment is of considerable
diagnostic value.
Solitary Fibrous Tumor
Previously called “benign mesothelioma” or “benign fibrous mesothelioma”
in the pleura and “fibroma” in the lung, solitary fibrous tumor is now
recognized as a soft-tissue tumor with a propensity to occur in the pleura
and, less commonly, in the lung, as well as other sites. The tumor is often
attached to the pleural surface by a pedicle. It may be small (1 to 2 cm in
diameter) or may reach an enormous size, but it tends to remain confined to
the surface of the lung. Grossly, it consists of dense fibrous tissue with
occasional cysts filled with viscid fluid; microscopically, the tumor shows
whorls of reticulin and collagen fibers among which are interspersed spindle
cells resembling fibroblasts.
Malignant Mesothelioma
Malignant mesotheliomas in the thorax arise from either the visceral or the
parietal pleura. Though uncommon, they have assumed great importance in
the past few years because of their increased incidence among people with
heavy expo-sure to asbestos. In coastal areas with shipping industries in the
United States and Great Britain, and in Canadian, Australian, and South
African mining areas, as many as 90% of reported mesotheliomas are
asbestos-related. The lifetime risk of developing mesothelioma in heavily
exposed individuals is as high as 7% to 10%. There is a long latent period of
25 to 45 years for the development of asbestos-related mesothelioma, and
there seems to be no increased risk of mesothelioma in asbestos workers
who smoke. This is in contrast to the risk of asbestos-related lung carcinoma,
already high, which is markedly magnified by smoking. Thus, for asbestos
workers (particularly those who are also smokers), the risk of dying of lung
carcinoma far exceeds that of developing mesothelioma.
DIAGNOSIS
Medical history and physical examination are usually followed by more
specific diagnostic procedures.
Useful tests for the early detection and staging of tumors include:
Laboratory values.
Radiography.
Endoscopy.
Isotope scan.
CT scan.
Mammography.
MRI.
Biopsy.
Treatment and prognosis vary not only with stage but also with cell type. In
general, surgery, chemotherapy, and radiotherapy are offered according to
the stage, resectability, operability, and functional status.
Despite all the advances, the outcomes for lung cancer remain
abysmal. The key reason is that most patients are diagnosed with
advanced-stage disease. To improve outcomes, an interprofessional
team approach with close communication between the members may
perhaps lead to earlier diagnosis and treatment.
The definitive diagnosis and management of lung cancer is done by
the thoracic surgeon with collaboration with the radiologist and
pathologist.
After surgery, the patients are usually monitored by nurses for
oxygenation, ventilation, and pain. Since many of these patients are
smokers, they also have other comorbidities like heart disease and
peripheral vascular disease, which often presents with symptoms in
the post-operative period.
After surgery, patients need prolonged rehabilitation. Some may need
chemotherapy and radiation.
PHYSIOTHERAPY INTERVENTIONS
Physiotherapy interventions vary depending on the stage in disease
trajectory and timing relative to treatment.
The cornerstone of physiotherapy management in lung cancer should
be prescription and delivery of exercise intervention.
Physical activity and exercise are vital components targeting three
main aspects of the cancer continuum: prevention, mortality and
morbidity.
The American Cancer Society recommends that adults with cancer
engage in at least 150 minutes of moderate-intensity aerobic exercise
and two sessions of resistance exercise per week, which is the same as
the guidelines for the general adult.
The following are the guidelines of physiotherapy during
exercises
Frequency: refers to how often the exercise is performed.
Application in Cancer Patients: Cancer patients are generally
recommended to engage in aerobic activities 3-5 days per week and
resistance training 2-3 days per week.
Intensity: is the level of effort required during physical activity, often
measured as light, moderate, or vigorous.
Application in Cancer Patients: For cancer patients, moderate-intensity
activities are typically recommended (e.g., brisk walking). Intensity
should be monitored closely to avoid overexertion, especially for those
experiencing fatigue or undergoing treatments.
Time: refers to the duration of each exercise session.
Application in Cancer Patients: Sessions can range from 20 to 60
minutes depending on the patient’s fitness level and treatment side
effects. Shorter, more frequent bouts may be preferable for those with
limited endurance.
Type: refers to the kind of exercise performed, such as aerobic,
resistance, flexibility, or balance training.
Application in Cancer Patients: Aerobic exercises (like walking or
cycling), resistance training (light weights), and flexibility exercises
(stretching, yoga) are beneficial. The type should be selected based on
the patient’s abilities, preferences, and any contraindications related to
cancer treatment.
Exercises
Aerobic exercise and resistance training have a positive impact on lung
functioning including a reduction in airflow obstruction and clearing of
airways therefore the improved functional capabilities increase energy
levels and the release of sputum.
Pulmonary Rehabilitation programs is tailored to the individual who has
recently had e.g. lung surgery, with the aim of optimizing their
respiratory function and therefore their quality of life (QOL) and
participation in their everyday lives.
Exercise following surgery or treatment aims to restore physical status
(addressing loss of functional capacity and muscle strength, which may
occur during treatment) and to maximize function, physical activity,
psychological status and health-related quality of life in the long term.
Research shows positive results of physical exercises on cancer-related
fatigue, physical function, symptom distress, sarcopenia and health-
related quality of life (HRQoL).
Postural drainage and breathing exercises: After a lobectomy (excision
of a lung Lobe), the PT and PTA can provide postural drainage and
breathing exercises to assist with the recovery of lung tissue expansion
and vital capacity.
PREVENTION.
Smoking cessation: The best way to prevent lung cancer is to quit
smoking. The risk of getting diagnosed with lung cancer will decrease
the sooner an individual quits smoking. After 10 years of not smoking,
the chance of developing lung cancer decreases to half that of
someone who smokes.
Diet: Research suggests that eating a low-fat, high-fibre diet, including
at least five portions of fresh fruit and vegetables and whole grains
every day, can help reduce the risk of developing lung cancer, as well
as other types of cancer and heart disease.[9]
Physical Activity/Exercise: Studies show that higher levels of
physical activity may lower lung cancer risk. It is important to exercise
regularly, attempting to perform at least 150 minutes of moderate
intensity aerobic activity each week and incorporate muscle
strengthening activities two days per week
REFERENCES.
Battaglini, C., & Hackney, A. C. (2014). Exercise and Cancer
Survivorship: Impact on Health Outcomes and Quality of Life.
Courneya, K. S., & Friedenreich, C. M. (2011). Physical Activity and
Cancer.
Exercise and Cancer Survivorship” by Battaglini and Hackney (2014)
https://www.physio-pedia.com/Lung_Cancer.
Robbins and Cotran Pathologic Basis of Disease, 9 th edition.
Schmitz, K. H., et al. (2010). American College of Sports Medicine
Roundtable on Exercise Guidelines for Cancer Survivors. Medicine &
Science in Sports & Exercise, 42(7), 1409-1426
