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Neoplasia 1 + 2 Flashcards

1
Q

what is meant by the term neoplasm?

A

an abnormal growth of cells that persists after the initial stimulus is removed

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2
Q

what is oncology?

A

the study of tumours and neoplasms

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3
Q

what are the differnt types of neoplastic tumours?

A
  1. Benign
  2. Malignant:
    * primary site (from where it originates)
    * secondary (to where it has spread)
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4
Q

what is a benign neoplasm?

A

when gross and microscopic appearances are innocent
wont spread

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5
Q

what is a malignant neoplasm?

A

abnormal growth of cells that persist after initial stimulus is removed
invades sorrounding tissue + potential to spread to distant sites

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6
Q

what is meant by the term cancer?

A

malignant neoplasm

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7
Q

what is meant by the term metastisis?

A

malignant neoplasms have the ability to spread from primary site to a secondary site

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8
Q

what is dysplasia?

A
  • pre-neoplastic alteration in cells
  • reversible
  • have large hyperchromatic nuclei
  • high nuclear to cytoplasmic ratio
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9
Q

what are the main differences between benigns vs malignant neoplasm?

A

Benign:
* benign neoplasms remain confined to site of origin
* usually harmless (but dependent on location)
* pushing outer margin + grow within a capsule
* resembles the parent tissue - well differntiated

Malignant:
* malignant neoplasms have the potential to metastasise + infiltrate other tissues
* have an irregular outer margin
* may have ulcerations and necrosis
* how much it resembles parent tissue depends on how well it differentiates

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10
Q

what are malignant neoplasm cells which dont resemble parent tissue called?

A

anaplastic

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11
Q

what is meant by the term differntiation and what are the different types ?

A

process of becoming different by growth or development

benign neoplasms are well differentiated - uniform cells

malignant neoplasms can vary from well differentiated to poorly differentiated - fewer uniform cells

clinicians use grade as a synonym for differntiation:
1. grade 1 = well differentiated
2. grade 2 = moderately differntiated
3. grade 3 = poorly differentiated

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12
Q

what are the classic features of poorly differntiated malignant neoplasms?

A
  • increasing nuclear size
  • increasing nuclear : cytoplasm
  • increased nuclear staining
  • increased num of mitotic figures
  • abnormal mitotic figures (mercedes benz symbol)
  • variation in size and shape of cells and nuclei
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13
Q

what is the difference between dysplasia and neoplasm?

A

dysplasia refers to any changes within epithelial layer
once basement membrane is infiltrated then it is a malignant neoplasm

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14
Q

what are the different stages of dysplasia?

A

no.1 Dysplasia: reversible
* increased nuclear size
* loss of maturation towards surface of epithelia
* loss of keratin

no.2 Carcinoma in situ: irreversible
* full thickness dysplasia - all epithelia affected
* hasnt infilitrated basement membrane

no.3 Invasive carcinoma: irreversible
* infiltrates basement membrane
* malignant tumour

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15
Q

what is the CIN scale?

A

scale used to show how poorly differentiated epithelial surface is in cervix:
* CIN 1 = only the lower 1/3 of epithelia is showing classical features of poor differentiation
* CIN 2 = lower 2/3 of epithelial is showing classical features of poor differentiation
* CIN 3 = entire epithelia is showing classical features of poor differentiation

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16
Q

why do we get neoplasia?

A
  • carcinogenesis
  • non-lethal genetic damage
  • accumulated mutations in somatic cells
  • mutations are caused by initiators - mutagenic agents
  • promoters that cause cell proliferation
  • tumour forms by clonal expansion of a single precursor cell that has incurred genetic damage
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17
Q

what are the different initiators?

A

Chemicals:
* smoking
* alcohol

Infections agents:
* HPV

Radiation

Inherited disorders

18
Q

what happens in the process of “progression”?

A
  1. start of with one cell which has a mutation
  2. this cell divides forming new monoclonal cells with the same mutation (if all cells originate from one single cell they are known as monoclonal)
  3. as time progresses these cells pick up new mutations which make them better adapted to survive
19
Q

which genes are affected in neoplasms?

A
  1. growth promoting proto-oncogenes
  2. growth inhibiting tumour supressor genes
  3. genes that regulate programmed cell death (apoptosis)
  4. genes involved in DNA repair

to cause a neoplasm you likely need more than one affected gene

20
Q

what are the impacts of mutations in proto-oncogenes?

A
  • growth promoting genes - cause cell proliferation
  • mutations can affect the normal function of these genes or give them a new function - this is known as a “gain of function” mutation
  • mutations can permanently turn these proto-oncogenes on so it results in uncontrolled growth
  • only need 1 allele to be affected
21
Q

what are the impacts of mutations in tumour supressor genes (TSG)?

A
  • normal function is to stop cell proliferation
  • mutations cause loss of function
  • cells continue to grow and no longer undergo apoptosis
  • most common mutation occurs in the TB 53 gene
22
Q

what are the impacts of mutations in apoptosis regulating genes?

A

abnormalities in apoptosis so cells dont undergo apoptosis and enhanced survival of cells

23
Q

what are the impacts of mutations in DNA repair genes?

A
  • loss of function mutations
  • genetic damage to cells isnt detected so cant be repaired
  • affected cells acquire mutations at an accelerated rate - this is AKA “state of mutator phenotype”
24
Q

how can you name benign neoplasms?

A

benign tumours generally end in -oma

25
Q

how can you name malignant neoplasms?

A

if epithelial end in -carcinoma
if sarcoma end in -stromal
exceptions to this rule:
* malignant neoplasm of testis is called a malignant teratoma

26
Q

what is meant by the term invasion?

A

breach of the basement membrane with progressive infiltration and destruction of sorrounding tissue
(not dysplasia)

27
Q

how do malignant neoplasms spread around the body?

A
  1. grow and invade at primary site
  2. enter transport system and lodge at a secondary site
  3. grow at secondary site to form a new tumour in a process called colonisation (colonisation has low success rate since they need perfect conditions to multiply)
28
Q

what does a carcinoma cell need to invade sorrounding tissue?

A
  • altered adhesion - reduced expression in E-cadherin and integrin
  • stromal proteolysis - altered expression of matrix metalloproteinases (MMPs) which can degrade basement membrane
  • motility - changes to actin cytoskeleton

to allow for this spread epithelail cells take on a phenotype more similar to mesenchymal cells - this is known as “epithelial to mesenchymal transition”

29
Q

how does a cancer cell spread to a distant site?

A
  1. blood vesels (haematogenous spread)
  2. lymphatic vessels
  3. fluid in body cavities (transcoelomic spread)
30
Q

what determines the site of a secondary tumour?

A

basically the next closest area in which the blood vessels, lymphatic vessels or fluid drains

31
Q

what is the seed and soil phenomenon?

A

the malignant cells at the secondary site need the optimum environment to survive and multiply

32
Q

what are the typical ways in which carcinomas and sarcomas spread?

A

carcinomas tend to spread via lymphatic vessels first
sarcomas tend to spread via blood vessels

33
Q

what is metastatic disease to bone?

A
  • metastases are the most common malignant bone tumours
  • spread from a primary site due to haematogenous spread
  • majority of lesions are asymptomatic (pain is major symptom if they happen to be symptomatic)
34
Q

what are the most common neoplasms that spread to the bone?

A

breast
bronchus
kidney
thyroid
prostate

35
Q

which type of cancer causes osteosclerotic metastes in bone?

A

prostate cancer
osteosclerotic - production of bone

36
Q

how can malignant cells evade host defences?

A

in normal detection:
* tumour cells can be recognised by immune system as non-self and destroyed - mediated by cell mediated mechanisms
* tumour antigens are recognised by cytotoxic T cells and CD8

immunosupressed patients are at higher risk of developing cancers

malignant cells can still evade patients who are immunocompetent by:
* reduced or loss of expression of histocompatability antigens
* expression of certain factors that suppress immune system
* failure to produce tumour antigen

37
Q

what are the local effects of neoplasia?

A
  1. direct invasion and destruction of normal tissue
  2. ulceration at surface leading to bleeding
  3. compression of adjacent structures
  4. blocking tubes or orifices
  5. raised pressure due to tumour growth or swelling (brain)
38
Q

what are the systemic effects of neoplasia?

A
  1. increased tumour burden results in parasitic effect on host
  2. reduced apetite and weight loss
  3. malaise
  4. immunosuppression
  5. thrombosis
  6. production of hormone (usually benign neoplasia)
39
Q

what is paraneoplastic syndrome?

A

some patients with cancer show symptoms which aren’t explained by the anatomic distribution of the tumour or by production of hormones from which the tumour arises

important because:
* may show earliest sign of occult neoplasm
* can cause significant clinical problems and be fatal
* can mimic metastatic disease

40
Q

what are examples of paraneoplastic syndrome?

A
  1. hypercalcaemia
  2. syndrome of inappropriate ADH secretion (IADHS)

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