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cranio exam 4 > head and neck cancer treatment options > Flashcards

head and neck cancer treatment options Flashcards

1
Q

most types of head and neck cancer begin in what type of cells?

A

squamous cells that line the moist surface inside the head and neck

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2
Q

what accounts for nearly 90-95% of head and neck cancer tumors?

A

squamous cell carcinoma

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3
Q

what can cause cancers in the back of the throat?

A

Oral human papilloma virus (HPV) (most common STD)–> oropharyngeal cancers

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4
Q

what is the key to increasing the survival rate for head and neck cancers?

A

early detection

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5
Q

head and neck cancers are —- of all cancer

A

3-5%

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6
Q

are women or men more affected by h & n cancers

A

men more than women

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7
Q

oral and pharynx cancer is —- of all h&n cancers

A

85%

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8
Q

chemical carcinogenesis

A

“multi-step” process

two hit theory–more than one agent for production of a tumor

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9
Q

viral associated etiopathogenesis

A

HPV types 16 and 18 – significant cause of OSCC in young people

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10
Q

there are about —– strains of HPV and —- are linked with h & n cancer

A

100 stains and 40-60 are linked with H & N cancer

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11
Q

how does HPV cause caner

A

HPV oncoproteins E6 and E7 bind and degrade tumor suppressor genes p53 and RB, preventing their protective function against cancer by loss of repair or apoptotic function

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12
Q

evolution of oral-oropharyngeal carcinoma

A
  • tobacco era
  • organ preservation
  • improvements in radiation
  • HPV
  • minimally invasive surgery
  • immunotherapy
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13
Q

intensity modulated radiation therapy

A
  • shapes the radiation beam to closely fit the area of the cancer
  • reduction in injury to surrounding tissue (salivary glands)
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14
Q

radiostic necrosis

A

an extraction site doesn’t heal in a person after radiation is given

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15
Q

cytotoxic therapy does what?

A

targets the pathway of tumor growth

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16
Q

TORS and TLM

A

trans-oral robotic surgery and transoral laser microsurgery

both are minimally invasive surgeries

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17
Q

radiotherapy has traditionally relied on — but now its evolving to use —-

A

CT and now they use PET scans more

18
Q

why do they use PET scans more?

A

it has superior tumor detection capability which will lead to better patient outcomes

19
Q

is there a difference between PET-CT and neck dissection?

A

survival is similar with both but doing PET involved less operations and it was more cost effective

20
Q

acute oral complications of radiation therapy

A

oral mucositis
infection
salivary gland dysfunction
taste dysfunction

21
Q

chronic oral complications of radiation therapy

A 
mucosal fibrosis and atrophy
xerostomia
dental caries
soft tissue necrosis
osteoradionecrosis
taste dysfunction
muscular/cutaneous fibrosis
infection
22
Q

LINAC

A
  • standard radiotherapy machine
  • multileaf collimator
  • form shapes to precisely fit area
  • tumor receives a very high dose and normal healthy cells nearby receive a much lower dose
  • each beam can vary in intensity so different doses of radiation can be given across a tumor
23
Q

IMRT can reduce the risk of —

A

long term side effects and xerostomia

24
Q

cell cycle specific anti-tumor agents

A
  • work against proliferating cells
  • bleomycin (G2)
  • antimetabolites (S)
  • taxanes (M)
25
Q

FDA approved cell cycle specific anti-tumor agents

A
  • abitrexate (methotrexate)–antimetabolite
  • blenoxane (bleomycin)–antibiotic (G2)
  • docetaxel (taxane) (M)
  • cetuximab (EGFR inhibitor)
26
Q

combination therapy

A

T: docetaxel (taxotere)
P: cisplatin (platinol)
F: fluorouracil (antimetabolite)

27
Q

cell cycle non-specific

A
  • against resting and proliferative cells

- alkylating agents (cisplatin)

28
Q

alkylating agents

A
  • cisplatin
  • form alkyl radicals which form covalent linkages with nucleophilicmoieties of DNA, RNA, and proteins
  • prevent cell division by cross-linking strands of DNA –> make irreversible changes ( destructive to rapidly proliferating cells)
  • mutagenic, teratogenic, carcinogenic, radiomimetic, oncolytic
  • vary in solubility, mem transport, pharmacokinetics, clinical utility
  • **myelosuppression/immunosuppression and susceptibility to infections are common
29
Q

antibiotics against tumors

A
  • bleomycin, doxorubicin and daunorubicin
  • produced by streptomyces species to form irreversible complexes with DNA which then inhibit cell division
  • work on different cell cycles as non-specific agents
30
Q

antimetabolites

A
  • methotrexate
  • structural resemblance to folic acid, purines, and pyrimidines (building blocks of DNA)
  • effect cell during S phase
  • interfere with rapidly growing cells–> oral manifestations prominent
31
Q

methotrexate

A

antimetabolite that inhibits conversion of DHF to THF by inhibition of dihydrofolate reductase enzyme
–results in decreased synthesis of thymidylic acid and inosinic acid thereby retarding DNA and RNA synthesis and protein synthesis is also inhibited

32
Q

what is a noted feature of antimetabolites?

A

oral manifestations (ulcerative stomatitis, glossitis, mucositis, gingivitis)

33
Q

taxanes

A
  • docetaxel
  • act by binding to cellular beta-tubulin, increase its polymerization and promote microtubule assembly
  • inhibits tubulin depolymerization
  • cells become arrested in M phase of cell cycle
  • sensitize cells to radiation
34
Q

vinka alkaloids

A

arrest cell division in metaphase by binding to microtubular protein tubulin that forms the mitotic spindles

35
Q

direct toxicities of cancer chemo

A

a. bone marrow–neutropenia, thrombocytopenia, anemia
b. gastrointestinal mucosa–mucositis, N/V/diarrhea, nutritional disturbances
c. oral mucosa
d. skin
e. hair follicles
f. gonads

36
Q

other toxicities of cancer chemo

A 
heart (doxarubicin)
liver (cyclophosphamide)
lung (**bleomycin)
cns (vincrestine)
kidney (methotrexate**)
37
Q

characteristics of ideal molecular targets

A
  • found on cancer cells
  • differentially expressed or differentially functional in tumor vs nontumor host tissues
  • specific to cancer cells
  • causally related to tumor cell viability, progression, or both
  • involved in several aspects of carcinogenesis pathway
  • measurable in diagnostic tumor material
38
Q

potential targets of targeted cancer therapy

A
  • extracellular blockade of HER/EGFR (human epidermal growth factor)
  • intracellular blockade of HER/EGFR
  • inhibition of growth inhibitory signals
  • evasion of programmed cell death and immortalization
  • angiogenesis
  • tissue invasion and metastasis
39
Q

options of targeted therapy

A
  • monoclonal antibodies (MAbs) **

- small-molecule inhibitors **

40
Q

what drug provides an extracellular blockade of HER/EGFR for treatment of H&N cancer

A

cetuximab

41
Q

adverse effects of antibodies as cancer therapeutics

A
  • anaphylaxis early in administration
  • hematological toxicity
  • neutropenia–> increased risk of infection
  • cardiac failure and pulmonary complications

cranio exam 4 (5 decks)

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