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EMS > Theme 5: Neoplasia - Part 5 > Flashcards

Theme 5: Neoplasia - Part 5 Flashcards

1
Q

What is pharmacokinetics?

A

what the body does to the drug

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2
Q

What are pharmacodynamics?

A

what the drug does the body

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3
Q

What is the study of pharmacogenetics?

A

The study of inherited genetic differences in drug metabolism pathways which can affect an individual response to drugs

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4
Q

What are the genetic variations that affect the metabolism of drugs?

A 
Changes in protein:
-gene amplification
-promoter polymorphisms
-translocations
-deletions, insertions
-single nucleotide polymorphism 
= altered outcome to treatment
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5
Q

What are the different ways genetic variations can affect drug metabolism?

A
  • absorption: drug might be excreted and not enter body
  • activation: most drugs prescribed are inactive and require enzymes to activate
  • altered target - can no longer bind to particular enzyme
  • catabolism (breakdown) -build up of activated drug might have toxic effects
  • excretion - if transporters are mutated functions will be impaired
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6
Q

What are ADRs?

A

adverse drug reactions - account for 6.5% of UK hospital admissions

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7
Q

How can genetics help tailored treatment?

A

start with broad diagnosis - everybody receives the same medication (30-60% effective)
then tailor treatment to match an individuals makeup and response - more effective and fewer side effects

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8
Q

How is Trastuzumab an example of personalised treatment?

A

A.k.a Herceptin

  • drug came about because it was found that 20% of breast cancers have over-expression of HER2
  • trastuzumab is a monoclonal antibody to the HER2 receptor
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9
Q

What are BRAF inhibitors?

A
  • melanoma is resistant to chemotherapy treatment
  • ~50% of melanomas have a somatic mutation in the BRAF gene
  • vemurafenib îs a BRAF inhibitor used in chemo
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10
Q

What is the most common type of genetic variant affecting drug metabolism?

A

SNPs

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11
Q

What does ADME stand for?

A

Absorption - how does drug get in
Distribution - where will it go?
Metabolism - how is it broken down?
Excretion - how does it leave?

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12
Q

what does TPMT do?

A
  • thiopurine methyltransferase

- inactivates certain drugs

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13
Q

What does azathioprine do?

A

immunosuppressant used in organ transplantation and autoimmune disease

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14
Q

What is aminoglycoside induced hearing loss?

A
  • G>A mutation causes non-syndromic hearing loss at later stages
  • maternal inheritance
  • accounts for 30% of tendency to amino glycoside toxicity
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15
Q

What did the PALoH study discover?

A
  • most babies admitted to NICU are given gentamicin
  • 1 in 500 babies have a genetic change that predisposes to complete irreversible hearing loss when given gentamicin
  • a rapid molecular test has been developed which can tell if babies are susceptible to this drug
  • saves 200 babies every year from going death
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16
Q

What is genetic counselling?

A

a communication process which deals with human problems associated with the occurrence, or the risk of occurrence, of a genetic disorder in a family

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17
Q

From what age can you have a genetic test?

A

From when your 18

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18
Q

What are examples of pre-natal genetic tests?

A
  • amniocentisis
  • transabdominal chorionic villus sampling
  • PGD (selective IVF) - pre-implanation genetic diagnosis
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19
Q

What are the causes of childhood deafness?

A
  • 50% genetic cause

- 50% other causes e.g prematurity, infection during pregnancy, childhood infection

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20
Q

What are the 5 most common types of cancer death in the world?

A
  1. Lung
  2. Colorectal
  3. Stomach
  4. Liver
  5. Breast
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21
Q

What % of patients with lung cancer are operable by the time they’re diagnosed?

A

20%

22
Q

What is going on at a cellular and tissue level that causes late presentation of lung cancer?

A

normal respiratory epithelium is changing to invasive malignant epithelium

23
Q

Explain the change of cell shape/type as lung cancer develops?

A
  1. In health, bronchial epithelial cells are pseudo-stratified
  2. changes to squamous metaplasia
  3. dysplasia - cells start to independently proliferate and grow uncontrollably
    low grade dysplasia - neoplastic cells grow just past the epithelium
    high grade dysplasia - whole epithelium can be replaced with neoplastic cells
  4. invasive carcinoma - neoplastic cells develop extra capabilities e.g movement (metastasis)
24
Q

Why are adhesion molecules lost in tumour cells?

A

so they can break away

25
Q

What is lavage?

A

washing out of a body cavity with water or medicated solution

26
Q

How can we subdivide lung carcinomas?

A
  1. non-small cell carcinomas (80% of lung cancers)
    - squamous carcinoma
    - adenocarcinoma
    - undifferentiated large cell carcinoma
  2. small cell carcinoma
    - most aggressive type of cancer, usually incurable
27
Q

What is lymphadenopathy?

A

swelling of lymph nodes

28
Q

What are some effects of a primary lung tumour?

A
  • cough e.g tumour irritating airways triggering cough reflex
  • haemoptysis - if invasive tumour damages vessels it can lead to coughing up blood
  • SOB e.g tumour blocks airway
29
Q

What are some effects of metastatic deposits?

A
  • SOB - tumour in pleural cavities cause an effusion which restricts lung expansion
  • lumps e.g nodes, skin, bones
  • neurological signs e.g destruction of brain tissue by deposits
  • SVCO - superior vena cava obstruction
30
Q

What are some systemic effects of lung cancer?

A
  • weight loss - loss of appetite, changes in metabolism etc due to circulating tumour products like cytokines
  • hypercalcaemia e.g from osteolytic metastases and/or parathyroid hormone related protein secretion by tumour cells
  • paraneoplastic syndromes
31
Q

From a cellular point of view, what may cause late presentation in lung cancer?

A
  • The process of gaining malignant genetic mutations takes years
  • Dysplasia, carcinoma and metastasis may take a long time to develop
  • The growing and invading can happen over weeks and years
  • Intraepithelial changes will almost always be asymptomatic
  • Early invasive phases will almost always be asymptomatic
32
Q

From an anatomical view point, what may cause late presentation of lung cancer?

A
  • Symptoms can be vague and non-specific
  • There is reserve capacity in the lungs so loss of function of one small area does not necessarily cause symptoms
  • Lack of pain fibres within the lung parenchyma means that a lung tumour within the centre of the lung may be asymptomatic
33
Q

Which tests can give you the diagnosis in a patient with a cancer of known primary? (CUP)

A
  • CT scans
  • blood tumour markers
  • biopsy of the tumour with H&E stain - tells you type of tumour
  • immunohistochemistry on the biopsy
  • molecular testing of biopsy
34
Q

Which test would be the most valuable in determining treatment options in advanced lung cancer - EGFR or KRAS mutation testing?

A

EGFR:

  • KRAS mutation is the most common aberration but we don’t have targeted treatment so there is no point testing for this mutation
  • EGFR mutation testing - we have targeted treatment
35
Q

What is the advantage of next generation sequencing our traditional sequencing technologies?

A
  • Able to test multiple targets simultaneously
  • Able to test multiple patient samples simultaneously
  • Cheaper to test - coming down in price all the time but still incredibly expensive
36
Q

What type of aberrations is FISH suited too?

A

gene rearrangements

37
Q

Which cancer patients should be routinely screened for lynch syndrome?

A

endometrial and colorectal cancer

38
Q

Explain the 6 steps in the metastatic cascade:

A
  1. detachment
  2. invasion
  3. intravasation - invasion into blood vessel
  4. evasion of host defences
  5. adherence to endothelium
  6. extravasation - tumour cells leave blood vessel
39
Q

What are the 4 changes to allow invasion?

A
  1. loss of cell-cell adhesion
  2. secretion of proteolytic enzymes
  3. increased cellular motility
  4. changes to cell-matrix interaction allows cell to move into the stroma
40
Q

What is a common site of metastasis from lung, brain, kidney, thyroid and prostate?

A

bone

41
Q

What is Gleason’s pattern scale?

A

cancerous cells in prostate cancer fall into 5 distinct patterns as they change from normal cells to tumor cells:
1. small, uniform glands
2. more stroma between glands
….
5. lack of or occasional glands, sheets of cells

42
Q

what does mining of hematite and uranium expose workers to?

A

radon - a known carcinogen

43
Q

What is EPIC?

A
  • european prospective investigation into cancer and nutrition
  • one of the largest cohort studies in the world
  • designed to investigate the relationship between diet, nutritional status, lifestyle and environmental factors and the incidence of cancer
44
Q

what are the categories of human carcinogens?

A
  • chemicals e.g PAHs, nitroamines
  • infectious agents e.g HPV, helocibacter pylori
  • radiation e.g UV light, radon
  • minerals e.g asbestos, heavy metals
  • physiological e.g oestrogen, androgens
45
Q

What does PAH stand for?

A

polycyclic aromatic hydrocarbons - class of chemical agents that are produced whenever organic material is burnt e.g toast, meat, fossil fuels, tobacco

46
Q

which cancers would the following agents cause:

  1. alcohol
  2. asbestos
  3. x-rays
  4. uV light
  5. oestrogen
  6. tobacco
  7. HepC
A
  1. pharynx, larynx, oesophagus, liver
  2. lung pleura
  3. bone marrow (leukaemia)
  4. skin
  5. breast
  6. mouth, lung, oesophagus
  7. pancreas, kidney, bladder
47
Q

How do promotors contribute to carcinogenesis?

A
  1. they can stimulate the two rounds of DNA replication required for mutation fixation
  2. they can stimulate clonal expansion of mutated cells, which enables the accumulation of further mutations
48
Q

How does ataxia telangiectasia come about?

A

inherited defects in the ATM gene involved in recombinational repair pathway
-these patients have elevated incidence of cancer

49
Q

What cells link chronic inflammation and cancer?

A
  • tumour-associated macrophages (TAMs)

- these cells are recruited by tumour cells and produce tumour necrosis factor-alpha (TNF-α)

50
Q

What does TNF-α do?

A

a cytokine that induces and maintains the inflammatory response and release oxygen and nitrogen species that can act as carcinogens

EMS (16 decks)

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