Flashcards for Med/Surg – Oncology
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Cancer
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2nd leading cause of death in US, only to CVD; men (lung, prostate, colorectal); women (lung, breast, colorectal); Higher in men & AfAm
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Cancer growth/spread
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Cell transformation by (inherited or acquired) genetic mutations of cellular DNA --> cells replicate (clone) --> cell proliferates abnormally (evading IC & EC) --> regulate processes/signals and defense mechanisms of body --> invade surrounding tissue to access blood & lymph --> travel
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Classifying/naming cancers
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by tissue of origin
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Metastasis
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spread of malignant cells from primary site to distant ones; can travel & "seed" other organs"; spread by lymphatic circulation (lodge in nodes or pass in circulation), hematogenous spread & angiogenesis spread ex: breast cancer --> spread to axillary, clavicular and thoracic channels
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Anaplasia
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Pattern of growth, cells lack characteristic and growth, shape and organization with respect to cells of origin = increased malignant potential
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Angiogenesis
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Growth of new blood vessels that allow cancer to grow
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Tumor-specific antigens (TSAs)
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any cell-surface antigen of a tumor that does not occur on normal cells of the same origin. ex: CEA & PSA
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Types of tumors (benigns, malignant, primary, secondary)
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Benign Tumor Slow growth rate, Grows within a capsule of fibrous tissue, No invasion of adjacent tissue = no mets, Cytology is uniform with well differentiated cells that look like origin cell Malignant Tumor High mitotic rate = rapid growth Not encapsulated = invades surrounding tissue, cytology poorly differentiated Primary Tumor Site of origin Secondary Tumor used to describe a metastatic tumor OR a new primary
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Decreased fibronectin
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malignant cell membranes less cohesive and less likely to adhere to adjacent cells
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Pleomorphism
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cells are large and irregularly shaped
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Mitosis in malignant cells need ___________________?
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glucose & O2 *If glucose & O2 unavailable --> use anaerobic metabolic channels
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Warburg effect
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Most cancer cells predominantly produce energy by a high rate of glycolysis (even in presence of O2) followed by lactic acid fermentation in the cytosol, (rather than by a comparatively low rate of glycolysis followed by oxidation of pyruvate in mitochondria as in most normal cells)
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Proteinases
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Destructive enzymes produced by malignant cells ex: collagenases (specific to collagen) plasminogen activators (s/t plasma)
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Carcinoma
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cancer of epithelial tissue of skin ex: basal cell - most common; cells lining the deepest part of the skin's outer layer squamous cell - often areas exposed to skin (lips, ears, neck)
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Sarcoma
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cancer of connective or supportive tissue
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Myeloma
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cancer of plasma cells
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Lymphoma
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cancer of lymphocytes
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Leukemia
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cancer of hematopoietic cells in bone marrow
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Carcinogenesis
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initiation, promotion & progression
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Carcinogenesis: initiation
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agents that initiate or promote cellular transformation referred to as carcinogens
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Carcinogenesis: promotion
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repeated exposure to promoting agents with increased expression and manifestation of abnormal genetic info (even after long periods of time)
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Carcinogenesis: progression
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demonstrate increased malignant behavior, stimulate angiogenesis & invade adjacent tissue
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TP53
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gene provides instructions for making a protein called tumor protein p53 (or p53). This protein acts as a tumor suppressor, which means that it regulates cell division by keeping cells from growing and dividing too fast or in an uncontrolled way. Implicated in 50% of non-inherited human cancers.
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Cancer risks
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increase with age (78% of Pt over 55); genetic lifestyle; environmental; medical
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Tumor grades & TNM
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I to IV, increase in severity T: extent of tumor N: lymph node involved? M: metasis involved?
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Causes of cancer
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viruses & bacteria; dietary factors; physical agents; hormonal agents; chemical agents; genetic/familial factors
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Virus & bacteria w/ cancer
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20% worldwide linked, ex: HPV Helicobacter pylori, associated with increased incidence of gastric malignancy leading to changes in mucosa
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Diet & cancer
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increased risk with fats, alcohol, salt-cured or smoked meats, nitrates and nitrite-containing foods, red & processed meats
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Physical agents & cancer
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Chronic inflammation, radiation/sun exposure, tobacco use
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Hormonal agents & cancer
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Endogenous changes or adm of exogenous hormones, ex: prolonged estrogen treatment
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Chemical agents & cancer
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tobacco smoke, workplace soot, pesticides, dyes, all alter DNA structure in body sites
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Genetics/familiar factors & cancer
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extra/too few chromosomes
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Cancer prevention
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primary: risk reduction, lifestyle and enviro (75% caused by) secondary: screening & early detection tertiary: monitoring for & preventing re-occurrence
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Cancer lab studies to guide treatment plans
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Evaluate baseline information prior to developing treatment plan: Marrow function Hepatic function Renal function Tumor Lysis Universal Standard of Care Labs Complete blood count with differential Basic Metabolic Panel Hepatic Function Other Common Labs Coagulation panel Pancreatic Enzymes Lactate Dehydrogenase (LDH) Biomarkers
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Normal immune response
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T-cells recognize TAA's as foreign and release cytokines that elicit various immune system actions --> 1. proliferation of cytoxic (cell-killing) T-cells capable of destroying cancer cells; 2. induce cancer cell apoptosis; 3. recruit addt'l immune system cells (B-cells produce antibodies, NK cells & macrophages) that destruct/degrade cancer cells
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Diagnosis
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Diagnosis of cancer requires tissue Histology = microscopic structure of tissues Cytology = structure and function of cells Select site most likely to obtain adequate tissue: Fine Needle Aspiration (FNA) Core needle biopsy Stereotactic biopsy Excisional Incisional CT-guided bx biopsy for tissue sample; images (CT - anatomical; PET - functional)
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Types of biopsy
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excisional; incisional (too large to be removed); needle method (suspicious masses, easily accessible)
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Treatment
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Prophylactic surgery - removal of non-vital tissue/organ to prevent increased risk of development Palliative surgery - cure not possible, relieving symptoms Radiation - 60% of patient's receive
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Radiation therapy goals
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Goal of RT = deliver therapeutic dose of ionizing radiation to malignant cells of tumor while minimizing injury to the surrounding Prophylaxis; control; emergent treatment; palliation
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Types of radiation treatment
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electromagnetic - xrays & gamma rays particulate - electrons, beta particles, pro/neutrons external radiation - most common form; internal radiation - localized (HD, LD) Most lethal damage is due to DNA modification within cells of malignant and normal tissue, ionizing can directly break strands of DNA helix --> cell death
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Alterations due to radiation
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myleosuppression, thrombocytopenia (platelet decrease), stomatitis, xerostomia, mucositis, fatigue
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Chemotherapy
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antineoplastic drugs to destroy cancer cells by interfering with cell function, including replication/repair of DNA response impacted by: dose intensity, dose density (Refers to reducing time between doses), dose intensification
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Goals of chemotherapy
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Cure Control Palliation Neo-Adjuvant Treatment Adjuvant Treatment Chemoprevention Myeloablation
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Cell cycle
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G0: rest G1: RNA/protein synthesis S: DNA synthesis (cell specific agents, most affected here) G2: premiotic phase, DNA synthesis complete, mitotic spindle forms
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Myleoblation
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A severe form of myelosuppression. Myelosuppression is a condition in which bone marrow activity is decreased, resulting in fewer red blood cells, white blood cells, and platelets. It is a side effect of some cancer treatments. Also called severe myelosuppression.
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Adjuvant
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surgery -> chemo -> radiation
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Neo-adjuvant
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chemo -> surg -> radiation
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Concurrent
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chemo + radiation
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Symptoms of cancer
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early stage usually not painful; general fatigue, weakness, prolonged fever; HEENT (unresolved hoarseness, swallow difficulty, enlarged lymph, prolonged epistaxis); resp (non-resolved cough); chest/breast (size change, texture, edema, dimpling, nipple retraction); GI (pain, discomfort after eating, anorexia, abdominal pain); genitur (dysuria, hematuria); integ (new/change mole, non-healing lesion, thick/new lump); neuro (headache, seizure)
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C.A.U.T.I.O.N.
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C- change in bowel/bladder A- soreness doesn't heal U - unusual bleeding/discharge T - thicken tissue or lump I - Indigestion/difficulty swallowing O - obvious change in mole/wart N - nagging cough
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Cancer patient care examples
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Fatigue MOST COMMON side effect! Should be assessed at every visit Can affect QOL Common chemo adverse events and timing Acute, delayed and anticipatory CINV (Assessing fluid, electrolyte status) Mucositis Myelosuppression (Modifying risks for infection, bleeding) Fatigue Neuropathy Psychosocial distress (Assessing cognitive status) wet desquamation --> do NOT disturb blisters; apply non-adhesive to weep areas; Dry, Erythematous Areas lukewarm H2O; use prescribed cream/ointment; avoid rub/scratch; avoid sun/cold weather exposure; alopecia - educate, prevent scalp trauma; N/V - nutrition consultant, meds, prevent unpleasant taste/sight; cachexmia, anorexia...
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Cancer treatment complications & emergencies
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infection; sepsis (risk: neutropenia, hemat malignancies); bleeding; superior vena cava syndrome; spinal cord compression; PE &/or cardiac tamponade disscriminated intravascular coagulation tumor lysis syndrome
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Sepsis s/s
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altered mental status; hyper/o thermia; diaphoresis; decreased urine output; hypotension; tachy (cardia and penia); electrolyte imbalance; abnormal arterial blood gas; discriminated intravascular coagulation
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T cells
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Memory; suppressor; killer; helper
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Killer T cells
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cytotoxic, destroy abnormal body cells, stimulate Th cell release, release perforin (to form pores) *Nk act similarly, but killer T needs a self-MHC marker to attack Recognize antigens on surface of WBC (particular macrophages), enlarge & form clone T-cells, secrete interferon & cytokines (stimulating B-cells and Killer T cells) Immune related adv responses: hypophysitis, thyroiditis, adrenal insufficiency, pneumonitis, hepatitis, pancreatitis, motor and sensory neuropathoes, arthritis
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WBC Normal range
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4,500 - 11,00 mcL
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Platelet Normal range
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150,000 - 400,000 mm3
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akathisia
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restlessness
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bradykinesia
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slow, voluntary movement
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chorea
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rapid, jerky involuntary movement
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dyskinesia
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impaired ability to voluntarily move
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dysphonia
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difficulty in speaking due to a physical disorder of the mouth, tongue, throat, or vocal cords
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homonymous hemianopsia
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half visual loss
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micrographia
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small ineligible writing
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papilledema
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edema of optic nerve
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radiculopathy
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disease of spinal nerve root
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spondylosis
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degenerative change to disc and adjacent vertebral bodies
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Herniation of lumbar disc
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90-95% in L5 - S1, low back pain with motor/sensation impairment
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Post-polio syndrome
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weakness, fatigue, muscoskeletal pain, 80% of survivors experiencing pain (M&W)
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Brain tumors
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gliomas - most common meningiomas - 15% of all acoustic neuromas - on 8th cranial nerve, impacts hearing/balance
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Parkinson's
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slow progressing, nuero movement leads to disability, usually 50's (early as 30's)
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Huntington
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inherited, nerve cells in the brain break down over time; chronic, progressive; involuntary movement and dementia (midlife)
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Muscular dystrophies
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incurable, progressive weakness and wasting, inherited
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Degenerative disk disease
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Osteoarthritis of the spine, usually in the neck or lower back; (neurological compression); diagnosis w/ 3+ mos of pain
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Herniation of cervical intervertebral disk
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aging, occupational stress & spondylosis, can lead to spinal cord lesions; Symptoms may include dull or sharp pain in the neck or between the shoulder blades, pain that radiates down the arm to the hand or fingers, or numbness or tingling in the shoulder or arm.
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Adaptive v innate immune response
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Adaptive immune- has specificity and memory. Specificity - ability to recognize and respond to particular targets. Memory - second exposure to the same organism The adaptive immune response is much slower than the innate immune response.
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Immune related toxicity management
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Generally based on severity of symptoms Grade 1: supportive care; +/- withhold drug Grade 2: withhold drug, consider re-dose if toxicity resolves to ≤ Grade 1. Low dose corticosteroids (prednisone 0.5mg/kg/day or equivalent) if symptoms do not resolve within a week Grade 3-4: discontinue drug; high dose corticosteroids (prednisone 1-2mg/kg/day or equivalent) tapered over ≥ 1 month once toxicity resolves to ≤ Grade 1.
