Cancer Flashcards
Proliferation
Rate of proliferation = Rate of degeneration
Stop and go signals
Contact inhibition
normal cells respect boundaries of other cells and don’t grow into the territories
Telomerase
DNA telomere protein cap naturally gets smaller as cells divide, and stop once it reaches certain length
In cancer, telomerase enzyme adds them back so it keeps dividingC
Cell growth regulators
Proto-oncogens = promote growth (become oncogens in cancer and hyperactive proliferate)
Tumor suppressor genes = suppress growth (in cancer theye dont work anymore)
Carcinogenesis
Development of cancer
1) Initiation stage (mutation occurs)
- Mutation in cell from carcinogens, inherited, or error
Carcinogenes = chemical, radioactive or virus
When occurs, cell either dies, repairs or replicates and becomes cancerous
2) Promotion stage
Reversible where proliferation of altered cells, more likely to become cancer in prescence of promoting factors
E.g. obesity, dietary fat, cigarette smoking and alcohol
3) Progression stage
Increased growth of tumor, metastasis
Benign and malignant
Benign - grow slowly, well differentiated, does not spread (eg. moles, uterine fibrioids)
Malignant - grows rapidly, poorly differentiated, metastases occurC
Classification of cancer
i) Anatomical site = origin of tumor, solid or haematological
ii) Histological analysis (grading) = more differentiated, the more benign so how close they resemble the cells they come from
iii) Extent of disease (staging) = help guide treatment, location of cancer and metstasis (Stage 1 and 2 is more localized, 3 and 4 is difficult to control)
TNM classification
T = Tumor size
N = spread to lymph nodes
M = Metastasis
Side effects
i) Local
Benign can also cause local problems
Occlusion eg. colon cancer
Ulceration eg. invade other tissues
Pain esp in bone metastases and nerve pressing
Infarction - cancer cells become its own supply and rob blood from surrounding cells
ii) Systemic
Weight loss = cachexia as it rob nutrients
Bleeding from eroding blood vessels and necrosis
Anemia from less RBC production
Clinical manifestations
Pain - can be direct pressure, obstruction, destruction, infection, inflammation
Brain tumor = HA
Fatigue - weakness, lack of energy, constant hypermetabolic state
Cachexia - wasting syndrome, possibly because the body is fighting cancer and proinflammatory cytokines released (breaks down protein and fats)
Anemia, thrombocytopenia and leukopenia
Anemia = chronic bleeding, malnutrition, common in GI cancers
Leukopenia - tumor invasion of one marrow, high risk of infection
Paraneoplastic syndrome
Rare syndrome where substances released from tumor or immune response
= Fever, HTN, hypotension, hypoglycemia
Lymphatic system
Protects against disease/infection by filtering body fluids that leaked from putting back into the blood stream
Lymphocytes maturing
B lymphocyte = Bone marrow
T Lymphoctes = Thymus
Lymph nodes - filter the fluid in lymphatic system (neck, axillary, chest, abdomen, groin), swell during infections
Spleen - holds cells like macrophages
Thymus, bonemarrow, liver and tonsils as well
Hodkins lymphoma
Reed-Sternberg cells
- In lympho nodes
- Requires biopsy
Good prognosis
More common in men ages 15-30 and older than 55
Risk factors
EBV Virus, occupational virus, genetic, HIV
Clinical manifestation - weight loss, fatigue, weakness
- Fever
- No painful lymph nodes
Non-Hodkins lymphoma
More common, worse prognosis
Men older than 60
Risk factors
Genetic, toxin exposure, immunosuppressants/chemo
Same clinical manifestation
Frequent infection
Growth fraction
High growth fraction = tissues that have cells in active proliferation
Chemotherapy drugs more toxic
Low growth fraction = cells that are G0 phase, less receptive to cytotoxic cells
Chemotherapy barrier
1) Impossible to know when 100% of cancer cell kill
2) Drug resistance over time
3) Solid tumors respond poorly due to low growth fraction
4) Nearly impossible to completely kill every malignant cell
5) Cannot selectively target cancer cells (healthy cells die too)
6) Dosage limited due to toxicity
Chemo strategies
1) Intermittent therapy
- Chemotherapy at irregular interrvals to allow healthy cells to recover
- Only used when healthy cells regenerate faster than cancer cells
2) Combination therapy
- Usually 2 or more drugs used to
i) Reduce drug resistance
ii) Reduce toxic effects to healthy cells
iii) Increase cancer killing rate
3) Optimizing dosage schedules
4) Regional drug delivery
- If possible, direct chemo to area to reduce systemic effects
Neutropenia
ABC uunder 500 = Nadir
Nadir reached in 10-14 days
Begins to develop 2-3 days after dose
Must be monitored closely as signs of infection will be masked from no inflammation of WBC
NC
- LOW GRADE FEVER = emergency immediately
- Minimize contact with others, avoid crowds, hand washing
- Reverse isolation in hospital
- Reduce food w pathogens
Thrombocytopenia
Platelet below 150,000
Nadir in 14-21 days
Bleeding gums, epistaxis, brusing, hematuria, hemoptysis
NC
No anticoagulants, aspirin
Use soft-bristle brushes and electrical razor
IV insertion carefully
Caution with blood pressure cuff
Anemia
Fatigue, pallor, SOB
Less common due to 120 day span
Digestive tract dysfunction
i) Stomatitis
- 2-3 days after dose and continues up to 2 weeks after treatment
NC - Good oral care, risk of dehydration and malnutrition
ii) Diarrhea
- Destruction of epithelial lining of intestine
- Can lead to infection
iii) N/V
- Direct stimulation of CTZ - recall mallory-wiess tear, aspiration, fluid loss, etc
Types
1) Anticipatory - before
2) Acute - minutes/hours
2)Delayed - day after
NC - Antiemetic 30 min before
Alopecia
Hair loss as hair has high growth fraction
Starts 7-10 days after start, but hair will grow back after 1-2 months of stopping treatment
Reproductive toxicity
Teratogenic esp in first trimester, better after 18 weeks
Irreversible sterility in men = sperm bank?
Can cause amonrrhea, menopausal symptoms in women
Extraversion of vesicants
Cytotoxic are veiscants administered IV through central line due to rapid dilution by the blood
Extraversion is when drug leaks to the surround tissues = pain, infection, necrosis
Stop immediately in redness, swelling, blisters
Carcinogenesis
Ironically, cytotoxic drugs can cause cancer by damaging DNA
Occurs yas after treatment
More likely with akylating agents - cyclophasmide
Erythropoietin
Stimulate RBC production in bone marrow
IV/Subcut
Rarely given, only in palliative circumstances as it increase of MI,s troke and death
May accelerate tumor growthGi
Filgrastim (Neupogen)
Elevate neutrophil count
Decrease risk of infection
No major side effect yay!
IV/Subcut
Oprelvekin (Neumega)
Stimulate platelet production and increase synthesis of megakaryocytes
Subcut
Cyclophasmide
Alkylating agent
Cell cycle non-specific
MOA - Destroy DNA in cancer cells
AE
- Hemorrhagic cystitis and acute bladder injury
- Carcinogenesis
NC
- Non-vesicant!! can be PO or IV
- Drink loads of fluid
- Monitor for hematuria, painful uriantion, etc.
Methotrexate
Antimetabolite - Folic acid analog
S-phase
MOA - Prevent conversion of folic acid that is needed for DNA synthesis
AE
- Pulmonaruy fibrosis - persistent dry cough, hypoxia, SOB
Leucovorin Rescue
Leucovorin rescue
Calcium folinate
MOA - Reduced form of folic acid that bypasses the metabolic block of methotrexate to reduce risk of healthy cell death
Used in methotrexate after 24 houts
Will NOT save cancer cells!
Also in fluororacil
Fluorouracil
Antimetabolite - Pyramidine analog
S-phase
ADJUNCT for solid trumors
MOA - Inhibit synthesis of DNA/RNA
NC - IV
Doxorubicin
Antitumor antibiotic
Non-specific
MOA - Isolated from streptomyces to injure cells DNA
AE
- Cardiotoxic = fatal HF
I) Acute - arrythmias approx. 2 weeks
ii) Delayed - HF secondary to cardiomyopathy months/years after
- Severe myelosuppression
NC
- IV, only for cancer
Bleomycin
Antitumor antibiotic (non-anthracycline derivative)
G2 Phase
MOA - Injure cells by binding to DNA and distorting it
AE
- Pneumonitis that can become fibrosis and death (persistent cough, hemoptysis, low O2)
- Not very myelosuppressive
NC - Parenteral IM IV or subcut
Vincristine
Mitotic inhibitor
M phase
MOA - Periwinkle pland Madagascar periwinkle to distribt mitosis microtubules that separate the chromosomes
AE
Peripheral neuropathy
- Less myelosuppression!
Paresthesia, weakness, sensorry loss, decreased reflexes
NC
Vesicant!!! IV
Paclitaxel (Taxane)
Mitotic inhibitor
Late G2/M phase
MAO - Inhibit cell division
AE -
- Severe hypersentivity - hypotension, dyspnea, angioedema, uricaria (hives)
- Cardiotoxic - bradycardia, heart block, MI
- Peripheral neuropathy
NC - IV
Common NC
High alert 2 nursce check
Carcinogenic, teratogenic, mutogenic - hangle with PPE
Local injury if contact with eyes, skin o rmucous membranes
Body fluids are also cytotoxic waste
Tamoxifen
Antiestrogen
MOA - Premenopausal ER positive breast cancer
Block estrogen receptor on breast cancer cells to decrease rate of tumor growth
AE
- Hot flashes
- Fluid retention
- N/V
- Menstraul irregularities
- RISK OF ENDOMETRIAL CANCER!!!
- DVT/PE risk (thromboembolism)
NC
- not safe for pregnancy
- PO with surgery and radiation
- common gold standard
Anastrozole
Aromatase inhibitor
MOA - postmenopausal to block aromatase enzyme responsible of making estrogen
AE
Increase in MI/HF risk
Angina
Mood swings
Depression
NC
- PO once a day
- Treatment 2-5 yrs, sosible first use tamoxifen and then swap to this for less AE
Carcinogens vs promoting factors
Carcinogens - tobacco, asbestos, radon, UV rays, radiation, viral exposure
Promotinf - oobesity, sedentary, dietary fat, alcohol, tobacco
CAUTION
bowel/bladder, sore, bleeding discharge, lump, indigestion, warts/mole, nagging cough
ABCDE (MELEONOMA)
A - Asymmetry
B - Border irregular
C - Colour multicoloured
D - Diameter larger than 6 mm
E - Evolving/growing
Lymph nodes
Normal lymph nodes - Movable, discrete, soft, nontender
Abnormal lymph nodes
Cancer = Hard, unilateral, persistent, non-tender, fixed
Infection - BILATERAL!, enlarged, warm, TENDER, firm, movable
