Cancer Flashcards

1
Q

What are 4 Risk Factors and Underlying Causes for the Development of Cancer?

A
  • Age
  • Genetics
  • Environmental Exposures
  • Infection
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2
Q

Risk Factors and Underlying Causes for the Development of Cancer

What is the relationshipship between age and cancer?

A
  • As age increases, the risk of mortality increases
    • As you grow older, more likely to be exposed to mutations. The healing process slows and repair processes weaken
  • Different age ranges have different risks of cancer
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3
Q

Risk Factors and Underlying Causes for the Development of Cancer

What are the relationships between environmental factors and cancer?

A
  • Smoking
    • 30% of all cancer deaths in developed countries are caused by smoking
    • Lung cancer most common
  • Alcohol
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4
Q

Risk Factors and Underlying Causes for the Development of Cancer

What are the relationships between Infections and cancer?

A
  • Viruses associated with development of specific cancers
  • Recurrent infections. Reach a stage where body gets tired. Cancer results.
    • Papillomavirus
    • Epstein-Barr Virus
    • HIV
    • Hep B and C
    • H. Pylori
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5
Q

What is the Aim of Cancer Screening?

A
  • Aim to detect disease in asymptomatic individuals at an early stage and treat as early as possible and be least invasive to patient
  • Screening for breast, colon and cervical cancer is beneficial for certain age groups
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6
Q

When is a Diagnosis made for Cancer?

What does Final Diagnosis rely on?

Size of tumour?

A
  • Diagnosis made following screening, development of symptoms or incidental findings
  • Final diagnosis relies on an invasive tissue biopsy
  • Size of tumour and presence of cancer in lymph nodes suggests disease spread – important prognostic marker(s)
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7
Q

Describe how the extent of Disease is defined

A
  • Defining the extent of disease is the first priority after the diagnosis is made
  • Staging is a series of invasive and non-invasive tests
    • Clinical Staging
    • Pathologic Staging
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8
Q

In Staging, the Information used to define the disease is as what?

A
  • This information is used to define the disease as:
    • Localised (limited stage) or metastatic (advanced)
    • Goals of treatment for localised and metastatic disease are very different
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9
Q

What’s the most common system to Stage Disease?

A
  • Most common system is the TNM (Tumour, Nodes, Metastasis) system
    • T – Size of the Primary Tumour (T1 – T4)
    • N – Presence and Degree of Nodal Involvement (N0 – N4)
    • M – Presence or Absence of Metastatic Disease (M0 – M1)
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10
Q

What are the Goals of Cancer Treatment?

A
  • Cure – generally for localised cancers (short, strong therapy)
  • Extend life expectancy and enhance quality of life – generally for metastatic cancers (not short or strong – about the comfort of the patient and extending their life)
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11
Q

What is the Role of Adjuvant Therapy in Typical Cancer Treatment?

What are examples of this?

A
  • Given in association with primary treatment (usually surgery or radiotherapy)
  • Aim of increasing the cure rate by ablating any residual (undetected) microscopic tumour mass
  • Examples
    • Chemotherapy to shrink tumour, followed by surgery to remove the tumour
    • Chemotherapy may also be given following the surgery
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12
Q

What are the Specific Use of Surgery in Cancer Treatment?

A
  • Most effective cure (up to 40% can be cured with surgery alone but depends on location)
  • Few metastatic lesions can be removed that will result in cure of a patient with cancer
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13
Q

What are the Specific Use of Radiotherapy in Cancer Treatment?

Is it used alone?

Side effects are?

What type of cancers can be cured with Radiotherapy?

A
  • Physical form of therapy that destroy any tissue in its path
  • Can be used alone or in combination to cure localised tumours and to control the primary site of disease
  • Side effects are generally localised
  • Breast, Hodgkin’s Disease, Head and Neck, Prostate and Gynaecological cancers can be cured
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14
Q

Can Chemotherapy cure tumours?

What are the types of Chemotherapy?

A
  • Most solid tumours cannot be cured with chemotherapy alone
  • Types:
    • Cytotoxic e.g. methotrexate, fluorouracil, doxorubicin
      • Toxic to all cells
    • Hormonal
      • Tumours use hormones as growth factors
    • Targeted
      • Antibodies (monoclonal) or small molecules
      • Target genetic lesions specific to the cancer cells (e.g. imatinib, traztuzumab)
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15
Q

Combination Therapy is effective because it accomplishes 4 important goals not possible with single agent therapy. What are these 4 goals?

A
  • Provide maximum cell kill within the range of toxicity tolerated by the host for each drug
  • Provide a broader range of coverage (different mechanisms) of any resistant cell lines in the heterogenous tumour population
  • Prevent or slow the development of new resistant lines
  • Synergism
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16
Q

What are the Challenges of Combination Therapy?

A
  • Multiple toxicities with greater patient discomfort
  • Impact of dose effect
  • Complicated to administer
  • Expensive
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17
Q

What is the Importance of Dose in Chemotherapy Protocol Development?

A
  • Ideally: efficacious dose without toxicity
  • Dose-response curve for almost all anti-tumour agents is steep for therapeutic and toxic effects
  • Reducing the dose slightly can cause a reduction in therapeutic effectiveness – take care, otherwise favouring tumour to grow
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18
Q

What is the Importance of Frequency in Chemotherapy Protocol Development?

A
  • Ideally, continue treatment for maximum cell kill, but don’t want break for too long to allow tumour to regrow – caution for toxicity
  • A reduction in dose rate of therapy made a greater than 2-fold difference in complete remission rates
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19
Q

What happens to the Immune System when someone develops cancer?

A
  • Body’s immune system recognises and eliminates abnormal and malignant tumour cells from the body
  • Equilibrium between tumour cells and immune system can shift in favour of the tumour and leads to an immune response below the threshold required for tumour elimination and emergence of tumour cells
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20
Q

What is the Mechanism of Action of Immuno-oncology Agents?

A

Inhibits the inhibition of T-cell’s activity by the cancer cells

21
Q

Immunotherapy and Checkpoint Inhibition

  • What is CTLA-4?
  • What is CTLA-4 in cancer?
A
  • CTLA-4 is a negative regulator of T cell activation
  • CTLA-4 on T cells outcompetes CD28 for binding to B7 on APC’s which reduces full T-cell activation and ability to ‘fight’ cancer cells
  • CTLA-4 has been shown to be upregulated and present on the surface of T cells in melanoma and some other cancers
    • Ipilimumab is inhibitor of CTLA-4 – used in melanoma
22
Q

Immunotherapy and Checkpoint Inhibition

  • What is PD-1 and PD-L1?
  • What is PD-L1 on tumour cells?
  • What can Inhibitors of PD-1 and PD-L1 prevent?
A
  • PD-L pathway is a major receptor-ligand network that functions primarily to provide a co-inhibitory signal
  • When PD-1 on the T-cell binds to PD-L1 on the tumour cell, the T-cell becomes deactivated, allowing the cancer cells to evade immune attack
  • PD-L1 has been shown to be overexpressed on tumour cells
  • Inhibitors of PD-1 and PD-L1 can prevent the tumour cells from binding to PD-1, enabling the T-cell to remain active and coordinate an attack
    • Pembrolizumab, nivolumab are PD-1 inhibitors
    • Atezolizumab, avelumab are PD-L1 inhibitors
23
Q

Why do Immune Related Toxicities occur?

A
  • Immunotherapy enhances activity of immune system. When the immune system gets too effective, it may detect its own body as a foreign object
    • Usually due to enhanced T-cell activity and are similar to ‘autoimmune’ type conditions
24
Q

What are examples of irAEs?

A
  • Rash/mucosal irritation
  • Diarrhoea/Colitis
  • Hepatotoxicity
  • Pneumonitis
  • Endocrinopathies (test and monitor baseline thyroid function)
25
Q

What is the mainstay treatment of irAEs?

A
  • The mainstay of treatment is dampening the immune response through the prompt initiation of steroids and either delaying or ceasing subsequent doses
    • Exception is endocrinopathies – manage hyper/hypothyroidism
26
Q

Side Effects of Chemotherapy

What is Nausea and Vomiting Classified as?

A
  • Acute (within 24hrs of treatment)
  • Delayed (24hrs – 5 days post chemo)
  • Anticipatory (e.g. before chemotherapy)
27
Q

Side Effects of Chemotherapy

What are the 2 Mechanisms of Nausea and Vomiting?

A
  • Central Pathway - Brain
  • Peripheral Pathway - GIT
28
Q

Side Effects of Chemotherapy

Mechanisms of Nausea and Vomiting: Central Pathway - Brain

  • What is it involved in?
  • The dorsal vagal complex integrates sensory inputs of what?
  • Activation of?
A
  • Predominantly involved in the delayed phase of the chemotherapy-induced nausea and vomiting
  • The dorsal vagal complex integrates sensory inputs:
    • Emetic centre
    • Area postrema
    • Vagal afferent terminals
  • Activation of:
    • Abdominal muscles
    • Diaphragm
    • Stomach and oesophagus
29
Q

Side Effects of Chemotherapy

Mechanisms of Nausea and Vomiting: Peripheral Pathway - GIT

  • What is it Predominantly involved in?
  • What drugs can damage the GIT and how do they do this?
A
  • Predominantly involved in the acute phase of the chemotherapy-induced nausea and vomiting
  • Cytotoxic drugs can damage the GIT
    • Activate messages to the brain centre
    • Activates abdominal vagal afferents
    • Release serotonin from enterochromaffin
30
Q

Side Effects of Chemotherapy

Diarrhoea

  • Incidence
  • Dose
  • Treatment
  • What can it lead to?
  • What are the treatments?
  • Caution?
A
  • High incidence. Drug (5-FU, Irinotecan), dose and treatment schedule related
  • Multifactorial: mucosal damage, alteration of gut flora, altered fluid absorption, changes in motility
  • Can lead to malnutrition, weight loss, electrolyte imbalance, renal insufficiency and hospital admission if not controlled
  • Treatment: loperamide, other anti-diarrhoeal medication
  • Caution: Diarrhoea is cytotoxic for 7 days after chemo, close the lid and flush and leave lid down
31
Q

Side Effects of Chemotherapy

Constipation

  • What is it a result from?
  • Onset?
  • Management?
A
  • May be a symptom of an organic condition, a complication of systemic disease, or side effect of cancer treatment
  • Onset may be within days to weeks of commencement of therapy
  • Management:
    • Strict monitoring
    • Prevention is the best management
    • Aperients
    • Fluid Intake
    • Physical Activity
32
Q

Side Effects of Chemotherapy

Mucositis

  • What is it?
  • Where?
  • Result of?
  • Signs and Symptoms?
  • Management?
A
  • Inflammation, erythematous and ulcerative
  • Can affect the entire GIT
  • May be as a result of chemotherapy or radiotherapy
  • Signs and Symptoms:
    • Redness throughout the oral mucosa and severe ulceration
    • Oral discomfort and pain
    • Altered taste
    • Bleeding
    • Poor nutritional intake (and subsequent weight loss)
    • Increased risk of opportunistic infections
  • Management:
    • Anaesthetics – lignocaine viscous
    • Antimicrobials – abx, mouthwash
    • Antioxidants and vitamins – vit E
    • Antiseptics - Chlorhexidine
    • Coating agents – Sucralfate
    • Corticosteroids – dexamethasone mouthwash
    • Cryotherapy – ice chips
33
Q

Side Effects of Chemotherapy

What are the Effect on RBC

  • Function
  • Half-life of formed element
  • Effect on chemotherapy
  • Treatment (if indicated)?
A
  • Function: Carry Oxygen
  • Half Life: 120 days
  • Effect on Chemotherapy: Little effect on single cycle, Multiple Cycles leads to anaemia
  • Treatment (if Indicated): Blood transfusion
34
Q

Side Effects of Chemotherapy

What are the Effect on WBC

  • Function
  • Half-life of formed element
  • Effect on chemotherapy
  • Treatment (if indicated)?
A
  • Function: Fight infections
  • Half-life of formed element: 8 hrs
  • Effect on chemotherapy: Significant acute effects
  • Treatment (if indicated): G-CSF
35
Q

Side Effects of Chemotherapy

What are the Effect on Platelets?

  • Function
  • Half-life of formed element
  • Effect on chemotherapy
  • Treatment (if indicated)
A
  • Function: Blood clotting
  • Half-life of formed element: 7-10 days
  • Effect on chemotherapy: Significant acute effects
  • Treatment (if indicated): Platelet Transfusion
36
Q

Side Effects of Chemotherapy

Infection

  • Signs
  • Treatment
    • Monotherapy
    • Combination
    • Skin infection
    • Low risk
A
  • Patients with cancer are more susceptible to infection
  • Signs include:
    • Fever, rigors, hypotension, tachycardia, neurologic changes etc.
  • Immediate, empirical treatment require
    • Broad spectrum abx (usually IV)
    • Monotherapy
      • Ceftazidime, Piperacillin/Tazobactam
    • Combination Therapy
      • Add aminoglycoside
    • Suggestive of Skin Infection
      • Add vancomycin
    • Low risk
      • Can use outpatient ceftriaxone or oral ciprofloxacin/amoxycillin-clavulanate
37
Q

Side Effects of Monoclonal Antibodies

A
  • Infusion reactions (mild)
  • Deficiency of the Target
    • Trastuzumab (anti HER-2)
      • Heart Failure
    • Rituximab
      • Reactivation of infections
    • Bevacizumab
      • Reduced wound healing
    • Cetuximab
      • Skin rash
38
Q

Side Effects of Targeted Therapy

A
  • Small molecule tyrosine kinase inhibitors are less specific for the target
  • Deficiency of the Target
    • Trastuzumab (anti HER-2)
      • Heart Failure
    • Rituximab
      • Reactivation of infections
    • Bevacizumab
      • Reduced wound healing
    • Cetuximab
      • Skin rash
  • Gastrointestinal (N+V)
  • Drug specific/idiosyncratic S/Es
    • Hepatotoxicity, skin rash incl. SJS
39
Q

What are the Risk Factors in Breast Cancer?

A
  • Increasing age
  • Older age at first child birth
  • Family history of breast cancer (especially at a young age)
  • Lifetime oestrogen exposure (e.g. prolonged HRT)
  • Early menarche/late menopause
  • Obesity
  • Excessive alcohol consumption
  • Previous exposure to thoracic radiotherapy
  • Genetic mutations
40
Q

Estrogen and Progesterone Receptors (ER and PR)

Roles of Biomarkers

  • What is the role of estrogen?
  • Increased expression?
  • Presence of these Receptors?
  • Most common in?
A
  • Estrogen can act as a growth factor
  • Cancers that use estrogen as a growth factor have an increased expression of hormone receptors
  • The presence of these on the surface of breast cancer cells (~50-70%), predicts the response (benefit) to targeted therapy
  • More common in older patient
41
Q

HER-2 (Human Epidermal Growth Factor 2 Receptor)

Roles of Biomarkers in Treatment of Breast Cancer

  • What is HER-2?
  • Prognosis?
  • HER-2 positive?
  • Methods to assess HER-2 status?
A
  • Trans-membrane growth factor receptor
  • Poor prognostic factor
    • Faster growing disease
    • Younger patients
  • Those with HER-2 positive tumours may benefit from more aggressive therapy
  • Methods to assess HER-2 status:
    • IHC, FISH, CISH
42
Q

In breast cancer, who are offered adjuvant therapy?

A

Adjuvant therapy offered to women at a high risk of relapse

43
Q

In breast cancer, the decision to use adjuvant therapy depends upon?

A
  • Chance of recurrence with no treatment/stage of disease
  • Patients physical status
  • Patient preference
44
Q

In breast cancer, the choice of adjuvant therapy treatments are guided by?

A
  • Patient age
  • ER/PR & Her-2 status
  • Likely toxicities from treatment
  • Patient factors e.g. comorbidities other meds
45
Q

Many cases of metastatic breast cancer occur in who?

A

Patients that were (unsuccessfully) treated for localised disease

46
Q

What are the aims of treatment in metastatic breast cancer?

A
  • Increase length of survival
  • Improve quality of life (palliative instead of cure)
47
Q

Is surgery indicated in metastatic breast cancer?

What is the preferred treatment?

A
  • Surgery isn’t indicated unless there can be a benefit from removal of specific lesions
  • Radiotherapy is the preferred treatment for specific lesions that are troublesome, such as bone metastasis
48
Q

What are the Chemotherapy Options for Metastatic Disease?

A
  • Hormonal
    • Tamoxifen
    • Aromatase Inhibitors
    • LHRH agonists
  • Cytotoxic
    • Broader treatment options
    • Taxanes, anthracyclines, vinorelbine, capecitabine, gemcitabine etc
  • Biological
    • Anti-HER-2 (trastuzumab, lapatinib)
49
Q

The chemotherapy options for metastatic disease are a treatment choice for who?

A
  • Patients with symptomatic disease
  • ER and PR negative disease
  • Disease that’s resistant to endocrine therapy