Patho 2 cancer – Flashcards

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etiology
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environmental diet biologic ETOH consumption and abuse viral- hepatitis B & C herpes-epstein barr HPV HTLV-1 retrovirus
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Environmental risk factors
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tobacco any source multipotent carcinogenic mixture linked to cancers of the lung, loer urinary tract, liver, kidney, pancreas, cervix uteri linked to myeloid leukemia
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environmental risk factors ionizing radiation
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emission from x rays, radiosotopes and other radioactive sources exposure causes cell death, gene mutations, and chromosome aberrations bystander effects poor gene repair changes in gap junction intrecellular communication
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environmental risk factors ultraviolet radiation
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causes basal cell carcinoma, squamous cell carcinoma and melanoma principal source is sunlight ultraviolet A and ultraviolet B promotes skin inflammation and release of free radicals
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environmental risk factors alcohol consumption
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risk factor for oral cavity, pharyn, hypo-pyarny, larynx, esophagus, and liver cancers cigarette/alcohol combination increases a persons risk
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environmental risk factors sexual reproductive behavior
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carcinogenic types of human papillomavirus high risk HPV the greater the number of partners the greater the risk for exposure
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environmental risk factors occupational hazards
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there are a substantial number of occupational carcinogen- asbestos, dyes, rubber, paint, explosives, rubber cement, heavy metals, air pollution, etc, radon also implicated- diet, electromagnetic fields
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cancer
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is the uncontrolled growth of abnormal cells in the body
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tumor
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new groth or neoplasm not all tmors are cancerous cancer means malignancy or neoplasm benign tumors however can be dangerous if the occlude or press aganst critical regions of the body
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benign
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slow growth well differentiated well defined capsules not invasive no metastasis
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malignant
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rapid growth undifferentiated not encapsulated invade surrounding regions metastasize
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tumor markers
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also known as biological markers found on the plasma membranes of tumors consist of : hormones, enzymes, genes, antigens, antibodies disease that have tumor markers that can be detected in the blood indicate a blood test for cancer
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tumor markers continued
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to screen individuals who are at risk of developing cancer to aid in the diagnosis of a specific type of tumor especially when symptoms indicate a tumor is present to track the progress of the cancer and treatment tumor markers: A fetoprotein AFP hepatic or germ cell cancers carcinoembryonic antigen CEA for colon, liver, pancreas, lung, breast, and so on prostate specific antigen PSA for prostate
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the genetics of cancer development
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caused by mutation of genes disease of aging multiple cell mutations over a long period of time after a number of mutations cancer will emerge have immortality telomeres protect and preseve chromosomes telomerase preserves telomere telomere found in ovaries, testes (germ cells) and in stem cells no other cells as they shorten cell dies cancer cells trigger telomerase and fail to die
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the cell cycle
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the number of cells produced = the number of cells that die number of cells remain constant G1 cell prepares to make DNA S-DNA synthesis is occuring G2- after DNA synthesis and in prepartion for mitosis M stage of mitosis after mitosis the cell returns to G1 and goes through the cycle again or can enter G0 swhere the cell remains dormant and doesn't replicate
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growth fraction
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cancer cells do not necessarily grow out of control they simply fail to die as predicted cells divide only when they are told to do so by growth factors some cells are going through the cell cycle others are not the ratio of cells at g0 to cells in proliferation if called the growth fraction tissue with large numbers of proliferating cells and few cells at the G0 phase has a high growth fraction tissue that has cells mostly at g0 has low growth fraction
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growth fraction continued
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chemotherapy agents tend to be much more toxic to tissue with high growth factors proliferating cells are sensitive to chemotherapy because these agents disrupts DNA synthesis or mitosis and most chemo agents are active against proliferating cells as opposed to those at g0. the problem is that the chemo agent will also be more toxic to normal cells with high growth fraction -bone, GI epithelium, hair follicles, sperm forming cells
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growth fraction cont.
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we cna predict how well tumors will respond to chemo based on the growth fraction solid tumors most common such as with breast, lung, colon cancers have low growth fraction and dont respond well other cancers leukemia Hodgkin lymphoma prostate have a high growth fraction respond much better cancers that dont respond well need additional treatment such as surgery while very few can be treated with chemo alone
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growth fraction 4
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we have no way yet to know when treatment is safe to stop we dont know when there has been 100 % cell kill once the numbers of cancer cells go below 1 billion they cant be detected by current technologies symptoms subside before all cancer cells are destroyed patient is said to be in remission
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cell differentiation
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grown up cells are called differentiated because they look different from one another you can tell a spleen cell from a skin cell
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differentiated vs undifferentiated cells
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differentiated working cells mutate form differentiated working tumors benign undifferentiated rapidly dividing cells mutate they form rapidly dividing tumors known as malignant
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neoplasia
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proliferate to form new tissue do not wait for signals from the body that the new tissue is needed ignore signals to stop dividing so not mature normally to do the job the tissue is supposed to do do not die off (apoptosis) as expected in order to keep the number of total cells constant
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naming tumors
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benign tumors- oma malignant tumors cancers epithelial tissue-carcinoma mesenchymal tissue- sarcoma
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tumor size
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T- tumor size and local spread of the primary tumor N- number of lymph nodes involved M- degree of metastasis
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metastasis
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vascular and lymphatic regional (local) distant predictable sites- lung to brain prostate to bone or liver breast to bone, lung, liver
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clinical manifestations of cancer
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pain- little to no pain associated with early stages of malignancy influenced by fear, anxiety, sleep loss, fatigue, and overall physical deterioration mechanism pressure, obstruction, invasion of sensitive structures, stretching of visceral surfaces, tissue destruction, and inflammation
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clinical manifestations of cancer fatigue
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subjective clinical manifestation most common complaint among pt tiredness, weakness, lack energy, exhaustion, lethargy, inability to concentrate, depression, sleepiness, boredom, and lack of motivation suggested causes sleep disturbance, biochemical changes from circulating cytokines, secondary to disease and treatment, psychosocial factors, level of activity, nutritional status and environmental factors
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syndrome of cachexia
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most severe form of malnutrition present in 80% of cancer pt includes- anorexia, early satiety, weight loss, anemia, asthenia, taste alteration, and altered protein, lipid and carbohydrate metabolism
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anemia
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a decrease in hemoglobin in the blood mechanism- chronic bleeding resulting in iron deficiency severe malnutrition medical therapies, or malignancy in blood forming organs
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leukopenia and thrombocytopenia
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direct tumor invasion to the bone marrow causes leukopenia and thrombocytopenia chemo drugs are toxic to bone marrow infection- risk increases when the absolute neutrophil and lymphocyte counts fall
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paraneoplastic syndromes
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symptom complexes that cant be explained by local or distant spread of the tumor or by the effects of the hormones released by the tissue from which the tumor arose affect 10% of pts may represent early sign the malignancy present can result in life threatening issues may interfere with treatment because they can mimic progression of the disease may include cushings anemia, polycythemia
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goals of treatments for cancers
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curative/control- surgery, chemo, radiation palliative-ongoing chronic care, pain sympotomatic management, hospice care
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pain control in cancer
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pt comfort is of prime importance knowing the type of pain is helpful to knowing how it should be treated family teaching as well as pt teaching is critical to the success of pain mangement intent in pain control is key
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pain control continued
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if death occurs however we hope along with the pt's level loved ones that it is peaceful, with dignity and no pain break through pain must be managed adjuvant analgesics may include antidepressants antiseizure meds can sometimes stop neuropathic pain pt self report of pain most important
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WHO analgesic ladder
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1. non opiate without adjuvant treatment 2. opioid for mild to moderate pain with or without nonopioid or adjuvant 3. opioid for moderate to severe pain with or without nonopiod and or adjuvant
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facial rating scale vs numeric rating scale
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FHS used for individuals with language or cultural barriers pain symptoms and reflections are the same in all cultures behavior and facial expressions might still be poor indications of pt pain status NRS alone may not be effective in cases f chronic pain pt description of pain might be needed, degree and intensity is important be alert to acute breakthrough
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drug classes
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cytotoxic agents hormones biologic response modifiers
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characteristics of neoplastic cells
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persistent proliferation invasive growth formation of metastases immortality
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tissue growth and chemotherapy
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chemotherapoy drugs are more toxic to tissue with high growth fraction bone marrow is becomes suppressed skin- tissue becomes fragile hair follicles- hair may fall out in response to drugs sperm- patients could loose ability to reproduce gastrointestinal tract- NV
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obstacles to chemo as a treatment
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cure demands 100% kill rate true early detection rare drug doses limited- dose cant exceed the amount that produces the maximally tolerated injury to normal cells agents lack selectivity some tumors respond poorly to chemo heterogeneity of the cancer cell- tumor are made up of multiple sub population of cells which behave and respond differently
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chemotherapy modalities
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intermittent chemotherapy combination chemotherapy regional drugn delivery- intra arterial intrathecal intracavity
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vinca alkaloids (vincristine)
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bone marrow sparing peripheral neuropathy, vesicant properties
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alkylating (nitrogen mustards)
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major adverse effects myelosuppression, NV diarrhea or constipation fatigue
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Platinum compounds (cisplatin)
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major adverse effects fdamage to bone marrow anemia
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antitumor antibiotics (adriamycin)
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marrow suppression, stomatitis, hair loss cardiotoxciity tissue damage with inflitration (vesicant properties with extravasation)
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biologicals
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newer agents alter host response to the cancer cells Interferon alpha 2a interferon alpha 2 b which are immunostiumlants
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chemo contin
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few other meds given during treatment with chem agents and or added as part of protocol for tx steroids (decadron) antiemetics (reglan) pain medications prn
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major toxicities of cancer chemotherapy
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bone marrow supporession neutropenia thrombocytopenia anemia stomatitis NV alopecia hyperuricemia extravasation constipation diarrhea reproductive toxicity carcinogenesis
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symptom management
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acute and chronic pain management / control NV fatigue anxiety cancer cachexia skin care prevention of infection
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