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Abberant Cell Growth and cancer , chemotherapy .pdf
1.
Introduction to Aberrant
cell growth Mehdi Hayat Khan Senior Nursing Instructor BSN,M.Phil Physiology,MSN* mehdisnc05@gmail.com
2.
Objectives By the end
of this session the learners will be able to, • Define the characteristics of the normal cell • Describe the characteristics if the cancer cells • Discuss the predisposing factors of the aberrant cell growth • Differentiate between malignant and benign tumor • Describe the TNM system • Explain proto oncogene and anti oncogene. Copyright © 2017 by Mehdi Hayat Khan
3.
Homeostasis • The “steady
state” that cell exists in normally. • An equilibrium of the cells with their environment for adequate function. Copyright © 2017 by Mehdi Hayat Khan
4.
Normal cell • Cells
are the smallest functional unit of the body • They contain structures that are strikingly similar to those needed to maintain total body function • The nucleus is the control center for the cell. It also contains most of the hereditary material. • The organelles, which are analogous to the organs of the body, are contained in the cytoplasm. • The cell membrane encloses the cell and provides for intracellular and intercellular communication, transport of materials into and out of the cell. Copyright © 2017 by Mehdi Hayat Khan
5.
Characteristics of the
Normal cell • Normal body cells have a number of important characteristics. • They can Reproduce themselves exactly • Stop reproducing at the right time • There is proper cell communication in between the cells • Stick together in the right place • Self destruct if they are damaged • Become specialized or 'mature Copyright © 2017 by Mehdi Hayat Khan
6.
Normal cell cycle Copyright
© 2017 by Mehdi Hayat Khan
7.
Cellular Adaptation Cellular adaptation
refers to changes made by a cell in response to adverse environmental change The adaptation may be • physiologic(al) (normal) • Pathologic(al) (abnormal) Adaptation can involve: ✓ change in cell size or number ✓ change to different type of cell Copyright © 2017 by Mehdi Hayat Khan
8.
On application of
Stress NORMAL CELL ADAPTATION CELL INJURY CELL DEATH Stress, demand Fails to adapt Injurious stress Copyright © 2017 by Mehdi Hayat Khan
9.
NORMAL <--->ABNORMAL Cellular Adaptations •
Atrophy • Hypertrophy • Hyperplasia • Metaplasia: simple columnar to stratified squamous (lungs) • Dysplasia: some loss of control as in cervix Copyright © 2017 by Mehdi Hayat Khan
10.
Types of Cellular
Adaptation Types of adaptation: 1. Atrophy 2. Hypertrophy 3. Hyperplasia 4. Dysplasia 5. Metaplasia. Copyright © 2017 by Mehdi Hayat Khan
11.
TYPES OF ADAPTATION Copyright
© 2017 by Mehdi Hayat Khan
12.
Atrophy: (cells shrink) •
Muscle atrophy is defined as a decrease in the mass of the muscle; • workload or adverse environmental conditions – Is adaptive and reversible – results in a decrease in cell size • Types and Causes – Disuse atrophy (paralysis) – Ischemic atrophy (kidney, heart) – Malnutrition atrophy (starvation) – Loss of endocrine stimulation (uterine, breast) – Denervation – Senile Atrophy (old age) Copyright © 2017 by Mehdi Hayat Khan
13.
HYPERTROPHY:( size of
cells) o In the size of cells which results in enlargement of the organs , without any change in the no. of cells o workload requirement of an organ part o Results in an increase in tissue mass o Seen in cardiac, skeletal, and muscle tissue o May be a normal physiologic response o as seen in an increase in muscle size with exercise o May be a pathological response as in myocardial hypertrophy from HTN or valve disease. Copyright © 2017 by Mehdi Hayat Khan
14.
HYPERPLASIA:( # of
cells) • Occurs due to a response from appropriate stimulus and ceases when stimulus is removed – An increase in NUMBER of cells • Restricted to cells capable of mitosis • Physiological hyperplasia – uterus and breast enlarge in pregnancy Copyright © 2017 by Mehdi Hayat Khan
15.
METAPLASIA o Transformation or
replacement of one adult cell type to another adult cell type (e.g., the change from columnar to squamous cells in respiratory tract, from squamous to columnar in Barrett esophagitis). o With continued smoke exposure, ciliated columnar cells are changed to stratified squamous cells o Metaplastic changes usually result from chronic irritation. o Metaplastic changes seem to the development of cancer, in some instances. Copyright © 2017 by Mehdi Hayat Khan
16.
DYSPLASIA:(ATYPICAL HYPERPLASIA) • Deranged
cell growth resulting in cells of varying size, shape, and appearance – May be associated with chronic irritation or inflammation – May be reversible if offending agent is removed • Dysplasia is considered A STRONG PRECURSOR OF CANCER!!! – Example: Cervical dysplasia – However, dysplasia is an adaptive process – may or may not lead to cancer • Decrease risk if irritation is removed or inflammation treated. Copyright © 2017 by Mehdi Hayat Khan
17.
Important Terminology • Anaplasia:
cells that lack normal cellular characteristics and differ in shape and organization with respect to their cells of origin; usually, anaplastic cells are malignant • apoptosis: programmed cell death • Oncology: Branch of medicine that deals with the study, detection, treatment and management of cancer Copyright © 2017 by Mehdi Hayat Khan
18.
Aberrant cell Growth Mehdi
Hayat Khan Senior Nursing Instructor BSN,M.Phil Physiology,MSN* mehdisnc05@gmail.com
19.
Cancer • A disease
resulting from the uncontrolled growth of cells, which causes malignant cellular tumors. • The second leading cause of death in developed countries. Copyright © 2017 by Mehdi Hayat Khan
20.
Cancer cells Cancer
(Neoplasia) • Cancer is a disorder of altered cell differentiation and growth. • The resulting process is called neoplasia, meaning “new growth,” and the new growth is called a neoplasm. Copyright © 2017 by Mehdi Hayat Khan
21.
Most Common Cancers •
In men, most common cancers are prostate, lung, and colorectal. • In women, they are breast, colorectal, lung, and uterine. Copyright © 2017 by Mehdi Hayat Khan
22.
Etiology/ Risk Factors
of cancer • Heredity (A hereditary predisposition to approximately 50 types of cancer has been observed in families. Breast cancer, for example, occurs more frequently in women whose grandmothers, mothers, aunts, or sisters also have experienced a breast malignancy) • Hormones (Hormones have received considerable research attention with respect to cancer of the breast, ovary, and endometrium in women and of the prostate and testis in men) • Immunological mechanisms (There is substantial evidence for the immune system’s participation in resistance against the progression and spread of cancer. The central concept, known as the immune surveillance hypothesis) Copyright © 2017 by Mehdi Hayat Khan
23.
Etiology/ Risk Factors
of cancer • Chemical agents (chemical carcinogens can be divided into two groups) 1. Direct-reacting agents, which do not require activation in the body to become carcinogenic. 2. Indirect-reacting agents, called procarcinogens or initiators, which become active only after metabolic conversion • Radiations (The effects of ionizing radiation in carcinogenesis have been well documented in atomic bomb survivors, in patients diagnostically exposed, and in industrial workers, scientists, and physicians who were exposed during employment). Copyright © 2017 by Mehdi Hayat Khan
24.
Etiology/ Risk Factors
of cancer 1. PHYSICAL AGENTS – Radiation – Exposure to irritants – Exposure to sunlight 2. CHEMICAL AGENTS – Smoking – Dietary ingredients – Drugs 4. Genetics and Family History • Colon Cancer • Breast cancer 5. Dietary Habits • Low-Fiber • High-fat • Processed foods • alcohol 6. Viruses and Bacteria • DNA viruses- Hepa B, Herpes, EBV, CMV, Papilloma Virus • RNA Viruses- HIV, • Bacterium- H. pylori 7. Hormonal agents • DES • OCP especially estrogen Copyright © 2017 by Mehdi Hayat Khan
25.
Copyright © 2017
by Mehdi Hayat Khan
26.
Normal Tissue renewal •
Normal tissue renewal and repair involves cell proliferation, differentiation, and apoptosis. Copyright © 2017 by Mehdi Hayat Khan
27.
Proliferation • Proliferation, or
the process of cell division, is an inherent adaptive mechanism for cell replacement when old cells die or additional cells are needed. • Cell proliferation is the process of increasing cell numbers by mitotic cell division. • In normal tissue, cell proliferation is regulated so that the number of cells actively dividing is equivalent to the number dying or being shed. • In humans, there are two major categories of cells: gametes and somatic cells. Copyright © 2017 by Mehdi Hayat Khan
28.
Apoptosis • Apoptosis is
a form of programmed cell death that eliminates senescent cells, cells with damaged DNA, or unwanted cells. Copyright © 2017 by Mehdi Hayat Khan
29.
Cell differentiation • Cell
differentiation is the process whereby proliferating cells become progressively more specialized cell types. This process results in a fully differentiated, adult cell that has a specific set of structural, functional, and life expectancy characteristics. • For example, the red blood cell is a terminally differentiated cell that has been programmed to develop into a concave disk that functions as a vehicle for oxygen transport and lives approximately 120 days. Copyright © 2017 by Mehdi Hayat Khan
30.
Differentiation Body cells can
be divided into two large groups: • The well differentiated neurons and cells of skeletal and cardiac muscle that rarely divide and reproduce, • Second is the progenitor or parent cells that continue to divide and reproduce, such as blood cells, skin cells, and liver cells. • A third category of cells are the stem cells that remain quiescent until there is a need for cell replenishment, in which case they divide, producing other stem cells and cells that can carryout the functions of differentiated cells. Copyright © 2017 by Mehdi Hayat Khan
31.
Differentiation • Cells can
be well differentiated, moderately differentiated, or poorly differentiated Grade of the cancer cell • The more normal a cancer cell looks, the lower its grade, • The more abnormal or less well developed a cancer cell is, the higher its grade • Low, medium or high grade. It is also called grades 1, 2, or 3, where grade 1 is low grade. Copyright © 2017 by Mehdi Hayat Khan
32.
Characteristics of Cancer
Cells • Cancer cells are different to normal cells in several ways. They don't die if they move to another part of the body and • Cancer cells don't stop reproducing (Unlike normal cells, cancer cells do not stop reproducing after they have doubled 50 or 60 times. Copyright © 2017 by Mehdi Hayat Khan
33.
Characteristics of Cancer
Cells • Cancer cells don't obey signals from other cells (Something in the cancer cells overrides the normal signaling system. • This may be because the genes that tell the cell to reproduce keep on and on firing. Or because the genes that normally tell the cell to stop reproducing have been damaged or lost. So the cancer cell keeps on doubling, regardless of the damage the extra cells cause to the part of the body where the cancer is growing) • Cancer cells don't stick together. • Cancer cells don't specialize, but stay immature. Copyright © 2017 by Mehdi Hayat Khan
34.
Tumors • Tumor is
a swelling that can be caused by a number of conditions, including inflammation and trauma, but more recently the term has been used to define a mass of cells that arises because of overgrowth. • Although not synonymous, the terms tumor and neoplasm often are used interchangeably. Copyright © 2017 by Mehdi Hayat Khan
35.
Tumor Growth Once cells
have an adequate blood supply, the rate of tissue growth in normal and cancerous tissue depends on three factors: 1. The number of cells that are actively dividing or moving through the cell cycle, 2. The duration of the cell cycle, and 3. The number of cells that are being lost relative to the number of new cells being produced. One of the reasons cancerous tumors often seem to grow so rapidly relates to the size of the cell pool that is actively engaged in cycling. Copyright © 2017 by Mehdi Hayat Khan
36.
Carcinogenesis Malignant transformation, or
carcinogenesis, is the process by which carcinogenic (cancer-causing) agents cause normal cells to become cancer cells is hypothesized to be a multistep mechanism that can be divided into three stages: 1. Initiation, 2. Promotion 3. Progression Copyright © 2017 by Mehdi Hayat Khan
37.
Carcinogenesis Initiation: Involves the
exposure of cells to appropriate doses of a carcinogenic agent that makes them susceptible to malignant transformation.) – Mutation of genetic structure – Has potential to develop into clone of neoplastic cells Copyright © 2017 by Mehdi Hayat Khan
38.
Carcinogenesis Promotion: involves the
induction of unregulated accelerated growth in already initiated cells by various chemicals and growth factors. Promotion is reversible if the promoter substance is removed. – Characterized by the increased proliferation of altered cells – Latent period • Initial genetic alteration to clinical evidence of cancer. Copyright © 2017 by Mehdi Hayat Khan
39.
Carcinogenesis Progression (the process
whereby tumor cells acquire malignant phenotypic changes that promote invasiveness, metastatic competence, autonomous growth tendencies, and increased karyotypic instability) – Characterized by increased growth rate of tumor as well as its invasiveness and metastasis Copyright © 2017 by Mehdi Hayat Khan
40.
Carcinogenesis Copyright © 2017
by Mehdi Hayat Khan
41.
Proto oncogenes • “Proto-oncogenes
are a group of genes that cause normal cells to become cancerous when they are mutated “(Adamson, 1987; Weinstein & Joe, 2006). • Mutations in proto-oncogenes are typically dominant in nature, • Mutated version of a proto-oncogene is called an oncogene. • Often, proto-oncogenes encode proteins that function to stimulate cell division, inhibit cell differentiation, and halt cell death. • All of these processes are important for normal human development and for the maintenance of tissues and organs. Copyright © 2017 by Mehdi Hayat Khan
42.
Oncogenes • Oncogenes, however,
typically exhibit increased production of these proteins, • Thus leading to increased cell division, decreased cell differentiation, and inhibition of cell death; taken together, these phenotypes define cancer cells. • Thus, oncogenes are currently a major molecular target for anti-cancer drug design. Copyright © 2017 by Mehdi Hayat Khan
43.
Spread of Cancer •
Malignant disease processes have the ability to allow the spread or transfer of cancerous cells from one organ or body part to another by 1. Invasion 2. Metastasis Copyright © 2017 by Mehdi Hayat Khan
44.
1. Invasion: • Invasion,
which refers to the growth of the primary tumor into the surrounding host tissues, occurs in several ways. • Mechanical pressure exerted by rapidly proliferating neoplasms may force fingerlike projections of tumor cells into surrounding tissue and interstitial spaces. Copyright © 2017 by Mehdi Hayat Khan
45.
2. Metastasis • spread
of cancer from primary (initial) site to distant site • Tumor cells travel through blood or lymph circulation to other body areas and invade tissues and organs there. • Primary tumor: The original site of the malignancy • Secondary tumor (sites): Areas where malignancy has spread i.e. metastasis (metastatic tumor) • Common sites of metastasis are lymph nodes, liver, lungs, bones, brain. Copyright © 2017 by Mehdi Hayat Khan
46.
2. Metastasis • 50
– 60 % of tumors have metastasized by time primary tumor identified • Lymph(most common) and blood are key mechanisms by which cancer cells spread. • Angiogenesis Copyright © 2017 by Mehdi Hayat Khan
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The steps of
metastasis Copyright © 2017 by Mehdi Hayat Khan
48.
Main Classifications of
Cancer • Lymphomas (cancers occurring in infection-fighting organs, such as lymphatic tissue). • Leukemia's (cancers occurring in blood-forming organs, such as the spleen, and in bone marrow). • Sarcomas (cancers occurring in connective tissue, such as bone). • Carcinomas (cancers occurring in epithelial tissue, such as the skin). Copyright © 2017 by Mehdi Hayat Khan
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Classification of the
Tumor • Neoplasm is an abnormal growth of tissue, and, when it also forms a mass, is commonly referred to as a tumor • Types of Neoplasm 1. Benign 2. Malignant Copyright © 2017 by Mehdi Hayat Khan
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Malignant and Benign Copyright
© 2017 by Mehdi Hayat Khan
51.
Cancer Prevention and
Detection 1. Primary Prevention 2. Secondary Preventions Copyright © 2017 by Mehdi Hayat Khan
52.
Cancer Prevention and
Detection • Reduce or avoid exposure to known or suspected carcinogens • Eat balanced diet • Exercise regularly • Adequate rest • Health examination on a regular basis • Eliminate, reduce, or change perceptions of stressors and enhance ability to cope Copyright © 2017 by Mehdi Hayat Khan
53.
Cancer Prevention and
Detection • Enjoy consistent periods of relaxation and leisure • Know 7 warning signs of cancer • Self-examination • Seek medical care if cancer is suspected Copyright © 2017 by Mehdi Hayat Khan
54.
Warning Signs of
Cancer Utilize the American Cancer Society 7 Warning Signals CAUTION • Change in bowel or bladder habits • A sore throat that does not heal • Unusual bleeding or discharge from body orifice • Thickening or lump in breast or elsewhere • Indigestion of difficulty in swallowing • Obvious change in wart or mole • Nagging cough or hoarseness Copyright © 2017 by Mehdi Hayat Khan
55.
Staging and Grading
of Tumors • Staging determines the extent of the spread of cancer. • Grading evaluates tumor cells in comparison to normal cells. Copyright © 2017 by Mehdi Hayat Khan
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TNM staging system It
is the system that classifies the various cancers into different anatomical forms, its regional lymph node involvement and distant metastasis. T: It is defined as the size of the primary tumor N: It tells the presence or absence of the tumor in the regional lymph nodes and lymph node drainage. M: It is the absence or presence to the distant spread or metastasis. Copyright © 2017 by Mehdi Hayat Khan
57.
TNM staging system “T”
Primary tumor: T0: No evidence of primary tumor T: Carcinoma in situ T1: Tumor < 2mm T2: Tumor >20 mm but less than 50mm T3: > 50mm T4: tumor of any size /to the chest wall or skin Tx: Primary tumor can not be assessed Copyright © 2017 by Mehdi Hayat Khan
58.
TNM Staging system “N”
Regional lymph nodes N0: No regional lymph nodes involvement N1: Movable level( axiliary involvement) N2: Mammary lymph nodes,( not palpable axillary) N3: additionally supraclavical lymph nodes are involved Nx: can not be assessed Copyright © 2017 by Mehdi Hayat Khan
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TNM staging system “M”
Distant Metastasis Mo: No distant metastasis M1: Metastasis present Copyright © 2017 by Mehdi Hayat Khan
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Tumor Grading or
histological classification • Grade 1: Differ slightly from normal; well differentiated • Grade 2: More abnormal; moderately differentiated • Grade 3: Very abnormal; poorly differentiated • Grade 4: Immature, primitive and undifferentiated cells; difficult to determine cell of origin Copyright © 2017 by Mehdi Hayat Khan
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Tumor Staging Copyright ©
2017 by Mehdi Hayat Khan
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Detection and diagnosis
of Cancer The earlier cancer is detected, the more likely it is to be controlled. • Tumor marker identification 1. PSA (Prostatic-specific antigen): prostate cancer 2. CEA (Carcinoembryonic antigen): colon cancer 3. Alkaline Phosphatase: bone metastasis • Fluoroscopy • Magnetic resonance imaging • Computed tomography • Ultrasonography Copyright © 2017 by Mehdi Hayat Khan
63.
Detection and diagnosis
of Cancer Direct Visualization a) Sigmoidoscopy b) Cystoscopy c) Endoscopy d) Bronchoscopy • PET Scan • Invasive Diagnostic Techniques • Biopsy is the most accurate diagnostic test for cancer. Copyright © 2017 by Mehdi Hayat Khan
64.
Goals of Cancer
Therapy 1. To cure the cancer – Complete eradication of malignant disease 2. To control the cancer – Prolonged survival and containment of cancer cell growth – Continued surveillance 3. To ease cancer symptoms (sometimes called palliation) – May involve terminal care if client’s cancer is not responding to treatment – Relief of symptoms associated with the disease Copyright © 2017 by Mehdi Hayat Khan
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Treatment Modalities for
Cancer Factors that determine treatment modality – Cell type – Location and size of tumor – Extent of disease – Grading and Staging of Cancer Copyright © 2017 by Mehdi Hayat Khan
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Treatment Modalities for
Cancer A variety of approaches, including 1. Surgery 2. Radiation therapy 3. Chemotherapy 4. Other therapies Copyright © 2017 by Mehdi Hayat Khan
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1. Surgery • Surgical
removal of the entire cancer remains the ideal and most frequently used treatment method Types of Cancer Surgeries: 1. Diagnostic Surgery – Biopsy • Excisional, • Incisional, and • Needle methods Copyright © 2017 by Mehdi Hayat Khan
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1. Surgery 2. Prophylactic
Surgery: • Prophylactic surgery involves removing nonvital tissues or organs that are at increased risk to develop cancer. • Colectomy, mastectomy, and oophorectomy are examples of prophylactic surgeries. 3. Palliative Surgery: • When cure is not possible, the goals of treatment are to make the patient as comfortable as possible and to promote quality of life 4. Reconstructive Surgery Copyright © 2017 by Mehdi Hayat Khan
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Prophylactic Surgery Copyright ©
2017 by Mehdi Hayat Khan
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Surgery Copyright © 2017
by Mehdi Hayat Khan
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2. Radiation Therapy –
Emission and distribution of energy 1. Curative – as in thyroid carcinomas, localized cancers of the head and neck, and cancers of the uterine cervix. 2. Control – when a tumor cannot be removed surgically or when local nodal metastasis is present, or it can be used neoadjuantly (prior to local definitive treatment) with or without chemotherapy to reduce the size of a tumor to enable surgical resection. Copyright © 2017 by Mehdi Hayat Khan
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2. Radiation Therapy 3.
Prophylactic – to prevent the spread of a primary cancer to a distant area (eg, irradiating the brain to prevent leukemic infiltration or metastatic lung cancer). 4. Palliative – to relieve the symptoms of metastatic disease. Copyright © 2017 by Mehdi Hayat Khan
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2. Radiation Therapy Two
types of ionizing radiation 1. Electromagnetic radiation (x-rays and gamma rays) 2. Particulate radiation (electrons, beta particles, protons, neutrons, and alpha particles) Administration of Radiation Teletherapy (external beam radiation) Brachytherapy (internal radiation), Systemic (radioisotopes), contact or surface molds. Combination of internal and external radiation can also be used. Copyright © 2017 by Mehdi Hayat Khan
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2. Radiation Therapy
(Side Effects) • Altered skin integrity is a common effect and can include alopecia • Alterations in oral mucosa secondary to radiation therapy include stomatitis (inflammation of the oral tissues), xerostomia (dryness of the mouth), • The entire gastrointestinal mucosa may be involved, and esophageal irritation with chest pain and dysphagia may result • radiation field, anemia, leukopenia (decreased white blood cells [WBCs]), and thrombocytopenia (a decrease in platelets) may result • The patient is then at increased risk for infection and bleeding until blood cell counts return to normal. • Systemic side effects include fatigue, malaise, and anorexia Copyright © 2017 by Mehdi Hayat Khan
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3. Chemotherapy • Chemotherapy,
antineoplastic agents are used in an attempt to destroy tumor cells by interfering with cellular functions, including replication. • Chemotherapy is used primarily to treat systemic disease rather than localized lesions that are amenable to surgery or radiation. Chemotherapy may be combined with surgery, radiation therapy, or both to reduce tumor size preoperatively (neoadjuvant), to destroy any remaining tumor cells postoperatively (adjuvant), or to treat some forms of leukemia or lymphoma (primary). Copyright © 2017 by Mehdi Hayat Khan
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3. Chemotherapy Classes of
Chemotherapy Drugs a. Alkylating agents • 1. Action: create defects in tumor DNA • 2. Examples: Nitrogen Mustard, Cisplatin b. Antimetabolites • 1. Action: specific for S phase • 2. Examples: Methotrexate; 5 fluorouracil • 3. Toxic Effects: nausea, vomiting, stomatitis, diarrhea, alopecia, leukopenia c. Antitumor Antibiotics • 1. Action: interfere with DNA • 2. Examples: Actinomycin D, Bleomycin • 3. Toxic Effect: damage to cardiac muscle Copyright © 2017 by Mehdi Hayat Khan
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3. Chemotherapy d. Miotic
inhibitors • 1. Action: Prevent cell division during M phase • 2. Examples: Vincristine, Vinblastine • 3. Toxic Effects: affects neurotransmission, alopecia, bone marrow depression e. Hormones • 1. Action: stage specific G1 • 2. Example: Corticosteroids f. Hormone Antagonist • 1. Action: block hormones on hormone-binding tumors (breast, prostate, endometrium; cause tumor regression • 2. Examples: Tamoxifen (breast); Flutamide (prostate) • 3. Toxic Effects: altered secondary sex characteristics Copyright © 2017 by Mehdi Hayat Khan
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Toxicity and side
effects • Acute toxicity – Vomiting – Allergic reactions – Arrhythmias • Delayed effects – Mucositis – Alopecia – Bone marrow suppression • Alopecia (hair loss) – Generally reversible – New hair often different color and texture – Wigs – Anorexia • Fatigue • Nausea & vomiting • Mucositis Copyright © 2017 by Mehdi Hayat Khan
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4. Other Therapies •
Targeted therapies or Biotherapies seek to minimize the negative effects on healthy tissues by disrupting specific cancer cell functions . • Other Therapies – Bone Marrow Transplantation – Gene Therapy – Unproven and Unconventional Therapies – Complementary and Alternative Medicine (CAM) Copyright © 2017 by Mehdi Hayat Khan
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Oncological Emergencies A. Pericaridal
Effusion and Neoplastic Cardiac Tamponade 1. Concern: compression of heart by fluid in pericardial sac, compromised cardiac output 2. Treatment: pericardiocentesis B. Superior Vena Cava Syndrome 1. Concern: obstruction of venous system with increased venous pressure and stasis; facial and neck edema with slow progression to respiration distress 2. Treatment: respiratory support; decrease tumor size with radiation or chemotherapy Copyright © 2017 by Mehdi Hayat Khan
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Oncological Emergencies C. Sepsis
and Septic Shock 1. Concern: Early recognition of infection 2. Treatment: prompt D. Spinal Cord Compression 1. Concern: pressure from expanding tumor can cause irreversible paraplegia; back pain initial symptom with progressive paresthesia and leg pain and weakness 2. Treatment: early detection and radiation or surgical decompression E. Obstructive Uropathy 1. Concern: blockage of urine flow; undiagnosed can result in renal failure 2. Treatment: restore urine flow Copyright © 2017 by Mehdi Hayat Khan
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Oncological Emergencies Hypercalcemia 1. Concern:
high calcium from ectopic parathyroid hormone or metastases. 2. Behaviors: fatigue, muscle weakness, polyuria, constipation progressing to coma, seizures. 3. Treatment: restore fluids with intravenous saline; loop diuretics; more definitive treatments Copyright © 2017 by Mehdi Hayat Khan
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Oncological Emergencies G. Hyperuricemia 1.
Concern: occurs with rapid necrosis of tumor cells as with chemotherapy; can result in renal damage and failure 2. Prevention and treatment with fluids and Alopurinol (Zyloprim) H. SIADH (Syndrome of Inappropriate Antidiuretic Hormone Secretion) 1. Concern: ectopic ADH production from tumor leads to excessive hyponatremia 2. Treatment: restore sodium level Copyright © 2017 by Mehdi Hayat Khan
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References • Porth, C.,
Matfin, G., & Porth, C. (2009). Pathophysiology: Concepts of altered health states (8th ed.). Philadelphia, PA:Wolters Kluwer Health/Lippincott Williams & Wilkins. • Smeltzer, S.C.C., Bare, B.G., Hinkle, J.L. and Cheever, K.H. eds., 2010. Brunner & Suddarth's textbook of medical- surgical nursing (Vol. 1). Lippincott Williams & Wilkins. • Grossman, S., Porth, C.M., Conelius, J., Gerard, S.O., Moriber, N., O'Shea, E.R. and Wheeler, K., 2014. Porth's pathophysiology: Concepts of altered health states. • LeMone, P., Burke, K., Dwyer, T., Levett-Jones, T., Moxham, L. and Reid-Searl, K., 2015. Medical-surgical nursing. Pearson Higher Education AU. Copyright © 2017 by Mehdi Hayat Khan
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