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IHD Part 2 306 > Oncology > Flashcards

Oncology Flashcards

1
Q

Dental implications of managing oncology patients: What does head and neck cancer involve?

A

anything below the base of the skull to the larynx

often need to lease with neurological and gastro if cancer spreads, or skin specialists

most commonly SCC

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2
Q

Dental implications of managing oncology patients: Why do exophytic growth cancers have a better prognosis than endophytic?

A

They grow out of the body so easier to remove

Endo more aggressive

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3
Q

Dental implications of managing oncology patients: Which two strains of HPV are most linked to HandN

A

HPV 16 AND 18

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4
Q

Dental implications of managing oncology patients: What are the aims of pre-treatment assessment?

A

Avoidance of unscheduled interruptions to primary treatment as a result of dental problems

Pre-prosthetic planning/treatment e.g., planning for primary implants/impressions for obturator

Planning for extraction of teeth which are of doubtful prognosis or are at risk of dental disease in the future and are in an area where there would be risk of osteoradionecrosis.

Extractions be carried out as early as possible in the patient journey, but as a minimum, at least 10 days prior to radiotherapy.

Planning for restoration of remaining teeth as required.

Preventive advice and treatment.

Assess potential for post treatment access difficulties e.g., trismus, microstomia.

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5
Q

Dental implications of managing oncology patients: What are the short term treatment side effects?

A

Mucositis: inflammation and ulceration of the mucosal lining of the oral cavity.

Infection: chemotherapy induced neutropenia makes the patient susceptible to bacterial, viral, and fungal infections. Oral candidal infections are extremely common following chemo or radiotherapy.

Xerostomia: dry mouth resulting from a decrease in the production of saliva as a result of radiotherapy.

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6
Q

Dental implications of managing oncology patients: What are the long term treatment side effects?

A

Altered anatomy: surgical ablation and reconstruction can cause permanent changes in oral anatomy making prosthetic rehabilitation difficult.

Rampant dental caries: Radiogenic dental caries is thought to be the result of reduced salivary flow as well as possible direct radiogenic damage to the amelodentinal junction by radiotherapy.

Trismus: may be caused by surgical scarring or by radiotherapy induced fibrosis of the masticatory muscles.

Mastication difficulties: if a significant number of opposing pairs of teeth are lost

Osteoradionecrosis: hypovascularity and necrosis of bone followed by trauma induced or spontaneous mucosal breakdown, leading to a non-healing wound.

Xerostomia - Challacombe

IMRT (Intensity-modulated radiation therapy ) - current method of radiotherapy which reduces the risk of xerostomia and may also do for osteoradionecrosis after tx

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7
Q

Dental implications of managing oncology patients: What preventative management for cancer patients is there?

A

Maintenance of good oral hygiene by effective tooth brushing; flossing daily.

Dietary Advice with regard to caries prevention.

Daily topical fluoride application (2800ppm or 5000ppm fluoride toothpaste) in custom-made trays or brush-on. Daily fluoride mouthrinse.

Daily use of GC Tooth Mousse TM containing free calcium (Aldi greek yoghurt cheap)

Saliva replacement therapy/ use of frequent saline rinses

Jaw exercises to reduce trismus (therabite).

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8
Q

Dental implications of managing oncology patients: What is the aetiology of HN cancer?

A 
Cigarettes
Alcohol
Lifestyle - lower immune function, diet, etc 
Genetics
Virus - HPV
Hormones
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9
Q

Dental implications of managing oncology patients: How do you rehabilitate soft tissue?

A 
Radial forearm flap (RFF); 
anterolateral thigh flap (ALT); 
latissimus dorsi; 
rectus abdominus
flaps based on the scapular/para-scapular axis.
Pedicle tongue flap
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10
Q

Dental implications of managing oncology patients: How do you reconstruct the mandible?

A

fibula flap
deep circumflex iliac artery flap (DCIA)
scapular flap
RFF

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11
Q

Cancer chemotherapy: What are the causes of cancer?

A
  • Environmental exposure
  • Viruses
  • Oncogenes
  • Tumour suppressor genes
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12
Q

Cancer chemotherapy: What is the treatment for cancer?

A
  • Surgery or
  • Radiotherapy - Mainly possible when tumour remains localised at the time of diagnosis.
  • Chemotherapy - once cancer metastasizes chemotherapy is required for effective cancer management.
  • Chemotherapy is often combined with radiotherapy to allow surgical resection to take place.
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13
Q

Cancer chemotherapy: How do chemotherapy drugs vary?

A
  • chemical composition
  • route of administration
  • type of cancer targeted
  • side effects
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14
Q

Cancer chemotherapy: What are the three types of chemotherapy?

A
  • Primary induction chemotherapy - when it is administered in patients with advance cancer for which no alternative treatment exists. Can be curative in only a small subset of patients who present with advance disease. (i.e. Hodgkin’s and non-Hodgkin’s lymphoma in adults or lymphoblastic leukemia in children).
  • Neoadjuvant chemotherapy - in patients with localised cancer for which alternative local therapies, e.g. surgery, exist but which are less than completely effective.
  • Adjuvant chemotherapy – as an adjuvant to local therapy such as surgery or radiation. Is effective in prolonging both disease-free and overall survival in patients with different type of cancer (i.e. patients with breast, colon gastric or non-small lung cancer).
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15
Q

Cancer chemotherapy: What is the main goal of antineoplastic agents?

A

The main goal of antineoplastic agents is to eliminate the cancer cells without affecting normal tissues
In reality, all cytotoxic drugs affect normal tissues as well as malignancies - aim for a favorable therapeutic index.

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16
Q

Cancer chemotherapy: What is the therapeutic index?

A

A therapeutic index is the lethal dose of a drug for 50% of the population (LD50) divided by the minimum effective dose for 50% of the population (ED50).

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17
Q

Cancer chemotherapy: how do you achieve cure?

A

a TOTAL CELL KILL must be tried
• Early diagnosis and early institution of treatment
• Combination chemotherapy
• Intermittent regimens
• Adjuvant and neoadjuvant chemotherapy occasionally

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18
Q

Cancer chemotherapy: What is the log-kill hypothesis?

A

It states that a given dose of chemotherapy kills the same fraction of tumor cells regardless of the size of the tumor at the time of treatment.

Chemotherapeutic agents kill a constant PROPORTION of tumour cell population (first order kinetics), rather than a constant NUMBER of cells, after each dose

  • Solid cancer tumours – generally have a low growth fractions thus respond poorly to chemotherapy and in most cases need to be removed by surgery
  • Disseminated cancers- generally have a high growth fraction and generally respond well to chemotherapy
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19
Q

Cancer chemotherapy: What do cell cycle specific drugs act on?

A

action on cells traversing the cell cycle

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20
Q

Cancer chemotherapy: What do cell cycle non specific drugs act on?

A

sterilize tumour cells whether they are cycling or resting in the G0 compartments.

21
Q

Cancer chemotherapy: What type of agents are CCNS?

A

Alkylating agents

  • Form highly reactive carbonium ion
  • Transfer alkyl groups to neucleophilic sites on DNA bases - causing cross linkage, abnormal base pairing, DNA strand breakage (reduces cell proliferation)

however Alkylating agents are carcinogenic in nature and can increase the risk of secondary malignancies

22
Q

Cancer chemotherapy: What are alkylating agents CCNS used to treat?

A

•Usedtotreatawidevarietyofhematologicandsolidtumour (i.e. ovarian cancer, brain tumours)
• Immunosuppressantaction
• Most of the adverse effects are generally dose-related and occur
primarily in rapidly growing tissues
• Bonemarrowdepression
• Nausea and Vomiting. Antiemetics are often given prior and after alkylating agents dosing

23
Q

Cancer chemotherapy: What type of alkylating agents are there?

A

Busulfan (Alkyl sulfuantes)
Mainly used for chronic myelogenous leukemia and other leukemias, lymphomas and myeloproliferative disorders. Controls tumour burden but can not prevents transformation or correct cytogenic abnormalities.

Lomustine (Nitrosoures)
Requires biotransformation to agents that have alkylating or carbamoylating activities. Can cross the blood brain barrier, mainly used to treat brain tumours.

Decarbazine (Triazenes)
Used in the treatment of various cancers, among them malignant melanoma, Hodgkin lymphoma, sarcoma, and islet cell carcinoma of the pancreas. Mainly given IV, is bioactivated in the liver.

24
Q

Cancer chemotherapy: how may you develop resistant to alkylating agents CCNS?

A
  • Increased activity of DNA repair enzyme
  • Increase metabolic inactivation of the drug
  • Decrease influx of the drug
25
Q

Cancer chemotherapy: What is though tot be the mechanism of action for platinum analogues CCNS?

A

Form highly reactive platinum complexes
Intra strand and interstrand cross-link
DNA damage
inhibits cells proliferation

26
Q

Cancer chemotherapy: What are the effects of Cisplatin?

A

Highly bound to plasma protein
Highly concentrated in kidney, intestines and testes. Mainly used for testicular, ovarian cancer and solid tumours (i.e. esophagus, gastric)

Poorly penetrates the BBB
Extensively cleared by the kidney and slowly excreted in urine

Adverse effects - emesis, nephrotoxicity, peripheral neuropathy and ototoxicit

27
Q

Cancer chemotherapy: What are antimetabolites CCS?

A

Act on intermediary metabolism of proliferating cells. Interfere with DNA and RNA growth by substituting for the normal building blocks of RNA and DNA (S phase).

Specifically designed and synthesized based on the knowledge of critical cellular processes involved in DNA biosynthesis

  • Folates antagonist (i.e. Methotrexate)
  • Purine antagonists (i.e. 6 Mercaptopurine)
  • Pyrimidine antagonist (i.e. 5 Fluorouracile)
28
Q

Cancer chemotherapy: What is the action of methotrexate?

A

Methotrexate (folic acid analogue)

Binds to the active catalytic site of dihydrofolate reductase (DHFR)

Inhibiting the synthesis of tetrahydrofolate (THF)

Interfering with formation of DNA, RNA and key cellular proteins

Poor brain penetration, remains in tissue longer than folate prolonging the inhibitor effect. Remains unchanged in urine

29
Q

Cancer chemotherapy: What are the effects of methotrexate?

A

Cytotoxic, mainly on bone marrow

Immunosuppressive, preventing clonal expansion of B and T lymphocytes

Anti-Inflammatory

30
Q

Cancer chemotherapy: What are the adverse effects of methotrexates?

A

Megaloblastic anemia, leuokopenia, alopecia, nephropathy

31
Q

Cancer chemotherapy: What are the properties of 6 Mercaptopurine?

A

6 Mercaptopurine (Purine antagonist )
Used mainly in childhood acute leukemia.
Inactive in its parent form, MUST be metabolized in its active form
By inhibiting the synthesis of purine nucleotides, its metabolites alter the synthesis and function of RNA and DNA
Does not cross the BBB
Adverse effect- nausea, vomiting, fatigue stomach/abdominal pain, fever.

32
Q

Cancer chemotherapy:What are the properties of 5 Fluorouracil?

A

5 Fluorouracil (Pyrimidine antagonist )

Used in stomach, colon, breast, ovaries, liver and skin cancer.

Inactive in its parent form, requires activation via a complex series of enzymatic reaction to ribosyl and deoxirybosil nucleotide metabolites in order to interfere with DNA’s synthesis.

Extreme short half life (5-10 min).

Adverse effect: nausea, vomiting, headache, mood disorder, cardiotoxicity, GI ulceration and bleeding, vein pigmentation. Local pain, burning, dermatitis.

33
Q

Cancer chemotherapy: How do Vinca alkaloids CCS work?

A

Natural products, are alkaloid that derive from the periwinkle plant Vinca Rosea.
Act by inhibiting tubulin proliferation, which disrupt assembly of microtubules. This results in mitotic arrest in metaphase, bringing cell division to a halt and ultimately leading to CELL DEATH.

34
Q

Cancer chemotherapy: When is Vincristine used?

A

Used for childhood cancers, Hodgkin’s and non-Hodgkin’s lymphoma, lymphosarcoma. The main dose-limiting toxicity is neurotoxicity, usually expressed as peripheral sensory neuropathy, autonomic nervous system dysfunction, constipation and ataxia.

35
Q

Cancer chemotherapy: When is Vinblastine used?

A

Used in Hodgkins disease and other lymphoma, breast and testicular cancer. Main adverse effects include bone marrow suppression, nausea, vomiting and alopecia.

36
Q

Cancer chemotherapy: What are Taxanes and how do they work?

A

Alkaloid ester derived from the Pacific yew (Taxus brevifolia) and the European yew (Taxus baccata)

Act by enhancing tubulin polymerization. This promotion of microtubules assembly occurs in absence of microtubules-associated proteins and guanosine triphosphate, resulting in inhibition of mitosis and cell division.

37
Q

Cancer chemotherapy: What is Paclitaxel?

A

TAXANE CCS

Used in a broad range of solid tumour (i.e. advanced breast cancer, ovarian cancer , head and neck, prostate and bladder cancer).

Extensively metabolized in the liver with 80% of the drug excreted in faeces. Dose reduction is required in patients with liver diseases.

Adverse effects include nausea, vomiting, hypersensitivity, myelosuppression, and hypotension.

38
Q

Cancer chemotherapy: How do anti tumour antibiotics work?

A

Bind to DNA through intercalation between specific bases

leads to

Block synthesis of RNA, DNA or both

DNA strand scission

Interfere with cells replication

39
Q

Cancer chemotherapy: Where do all cancer antibiotics now used come from?

A

All the cancer antibiotics now used in clinical practice are from the soil microbe Streptomyces

40
Q

Cancer chemotherapy: What is dOXORUBICIN used for?

A

Doxorubicin (Anthracycline)
Mainly used against breast, ovary, testicles, stomach, thyroid and bladder cancer. Often used in combination with other anticancer drugs. Generates free radicals leading to cardiotoxicity.

41
Q

Cancer chemotherapy: what is Mitomiycin C CCNS used for?

A 
Mitomiycin C (CCNS)
Highly toxic, used in resistant cancers of stomach, colon and rectum. Its metabolite act like alkylating agent that cross-links DNA. It is active in all phases of the cell cycle. It is the best available drug to use in combination with radiotherapy to attack hypoxic tumour cells
42
Q

Cancer chemotherapy: What is bleomycin CCS used for?

A

Bleomycin (CCS)
It is a small peptide, binds to DNA resulting in single- and double-strand breaks, leading to inhibition of DNA biosynthesis. Causes accumulation of cells in G2 phase. Used for lymphomas, head and neck cancer. Advantage can be given SC, IM or IV. Eliminated via renal excretion. Can lead to Pneumonitis, hyperpigmentation and spares bone marrow.

43
Q

Cancer chemotherapy: What are glucocorticoids used for?

A

Used in acute leukemia and lymphomas due to their marked lympholytic effect

44
Q

Cancer chemotherapy: whAT ARE ESTROGENS USED FOR?

A

Physiological antagonists of androgens, so used to antagonize the effect of androgens in androgen dependent prostate cancer

45
Q

Cancer chemotherapy: What are oestrogen antagonists used for?

A

Used in breast cancer. Selective Estrogen Receptor (ER) Modulators, or ER down regulator. Adverse effect, hot flushes, vomiting, menstrual irregularities.

46
Q

Cancer chemotherapy: What cancers commonly metastasise to the skeletotn?

A

multiple myeloma and metastatic breast, prostate, and thyroid cancers

47
Q

Cancer chemotherapy: What is spread of cancer to the bone associated with?

A

• pain,hypercalcemia,anemia,
• increasedriskofinfection,
• compression of the spinal cord and/or nerve
roots,
• decreased mobility and skeletal fracture (catastrophic)

48
Q

Cancer chemotherapy: What do bisphosphonates do?

A
  • Slow down the rate of growth of bone crystal and their resolution
  • Reduce morbidity from bone metastasis by reducing skeletal events.
  • Lower calcium levels.
  • After IV administration approximately 25–40% is excreted by the kidney, and the remainder is taken up by bone.
  • Poor oral bioavailability
  • As they bind to calcium in the diet can cause gastrointestinal toxicities such as nausea, vomiting, indigestion, oesophagitis, and diarrhea.
49
Q

Cancer chemotherapy: drug combination

A

..

IHD Part 2 306 (23 decks)

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