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Session 8 Flashcards

1
Q

What is a benign neoplasm?

A

A gross and microscopic appearance that is considered to be innocent (will remain localised and not spread to other sites)

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2
Q

What is a cancer?

A

A malignant neoplasm (abnormal growth of cells that persists after the initial stimulus is removed and invades surrounding tissue with the potential to spread to distant sites)

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3
Q

What is a metastases?

A

Malignant neoplasm that has spread to a new, non-contiguous site (completely separate)

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4
Q

What is dysplasia?

A

A pre-neoplastic alteration in which cells show disordered tissue organisation (reversible if lower grade)

  • Can get to the point where cells are malignant but not yet invasive
  • Malignancy prevented if detected early enough
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5
Q

What is an example of a non-neoplastic tumour?

A

Swelling due to inflammation (eg. abscess, haematoma)

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6
Q

Is neoplasia reversible?*

A

No

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7
Q

What is the difference between primary and secondary neoplasia?

A

Primary - has not spread (still at the original location)

Secondary - has metastasised to non-contiguous sites

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8
Q

How to tell a benign and malignant neoplasm apart?*

A

Benign:

  • Confined local area (no metastases) and can just be removed by surgery
  • Pushing outer margin
  • Location rarely dangerous
  • Have a ‘pseudocapsule’

Malignant:

  • Irregular, outer margin and shape
  • Ulceration and necrosis
  • Infiltrative
  • Metastases (patient becomes unwell)
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9
Q

What is differentiation and how does it apply to benign and malignant neoplasms?*

A

Differentiation: process of becoming different by growth/development

  • Benign closely remember parent tissue
  • Malignant neoplasms range from well to poorly differentiated
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10
Q

What are anaplastic cells?*

A

Cells with no resemblance to any tissue

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11
Q

What are the features of worsening differentiation?

A
  • Increased nuclear size + nuclear to cytoplasmic size
  • Increased hyperchromasia (nuclear staining)
  • Increased mitotic figures (abnormal DNA multiplying quickly)
  • Abnormal mitotic figures (Mercedes Benz)
  • Pleomorphism
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12
Q

Why can benign tumours be fatal sometimes?

A

Due to location (eg. brain) - skull is enclosed box, so increasing pressure causes symptoms

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13
Q

How do clinicians define differentiation?*

A

Grades: low grade is well differentiated, while high grade is poorly differentiated (have a poorer prognosis)

Differentiated cells are also likely to function very differently

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14
Q

What is a tumour?

A

Any clinically detectable lump or swelling

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15
Q

What is a neoplasm?

A

An abnormal growth of cells that persists after initial stimulus is removed

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16
Q

What is oncology?

A

The study of tumours and neoplasms

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17
Q

What is the difference between malignancy and hyperplasia and regeneration?*

A

Neoplasia is triggered by genetic alterations and grows uncontrollably. Hyperplasia and regeneration is programmed growth.

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18
Q

What is the Gleason’s pattern?*

A
  1. Small and uniform glands
  2. More stroma between glands
  3. Distinctively infiltrative margins
  4. Irregular masses of neoplastic glands
  5. Less than <10% gland formation, very high mitotic count, big variations in shape and size
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19
Q

Why do grades matter?*

A

Higher grade cancers have a poorer prognosis as they usually behave more aggressively and metastasise quicker

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20
Q

What is dysplasia?

A

Altered differentiation - progresses through grades and is a precursor to malignancy but is NOT YET INVASIVE

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21
Q

What is the difference between in situ and invasive disease?*

A

In situ disease HAS NOT BREACHED BASEMENT MEMBRANE and therefore cannot invade and metastasise

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22
Q

What is carcinoma in situ?*

A

Whole basement membrane epithelium thickness looks malignant but has not broken the BM so is not yet invasive

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23
Q

What can initiate neoplasia?

A
  • Chemicals (eg. smoking, alcohol, obesity)
  • Infectious agents (HPV and cervical carcinoma)
  • Radiation
  • Inherited mutations (BRCA1)
  • Spontaneous mutations
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24
Q

Why do people get neoplasia?*****

A
  • Accumulated mutations in somatic cells that are caused by mutagenic agents (initiators)
  • Promoters can then cause cell proliferation: differentiated cell replicates to create a bigger, neoplastic population
  • Tumours = clonal expansion of a cell that incurred genetic damage
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25
What is a monoclonal population?
A population that call came from the same single cell precursor
26
Why do people with genes get the cancers earlier?*
In germline mutations the neoplastic cells can miss out the steps of proliferation and then appear quicker
27
How does a neoplasm form from monoclonal cells?
Progression: accumulation of more mutations
28
What is progression?
Gaining more mutations that can give advantages (eg. autonomous growth to avoid checkpoints)
29
What genes are affected?
- Genes regulating apoptosis - Genes involved in DNA repair - Growth inhibiting tumour suppressor genes - Growth promoting proto-oncogene
30
What are proto-oncogenes?
Genes with multiple functions that participate in signalling pathways driving proliferation
31
How do proto-oncogenes mutate?
- Excessive increase in one/more normal function - Can have a gain-of-function mutation - Can encode oncoproteins that promote cell growth in absence of normal growth promoting signals (grow of own accord)
32
Why is cancer so common?
Only one oncogene needs to be mutated as they are dominant over normal counterpart of the gene
33
What is a tumour suppressor gene?
A gene that stops cell proliferation (tp53 more common; regulates cell cycle progression) - Most frequently mutates
34
How do tumour suppressor genes cause cancer?
- Recessive (both alleles damaged) - Loss of function mutation - Failure of growth inhibition
35
How do apoptosis regulating genes cause neoplasia?
Acquire abnormalities that result in less cell death and enhanced survival of cells with abnormalities
36
What are DNA repair genes?
Genes that are able to recognise and repair non-lethal genetic damage in other genes
37
How do DNA repair gene damages cause neoplasia?
- Loss of function Direct contribution - Impair ability to recognise and repair the cells - Affected cells acquire more mutations more quickly
38
What is a benign tumour called?
- Usually ends with -oma
39
What are epithelial neoplasms called?*
- Stratified squamous: squamous papilloma (if fingerlike projections) - Transitional cell papilloma - Adenoma/cystadenoma
40
What are the polyp names of benign neoplasms?*
Villous, sessile, tubular
41
What are epithelial neoplasms called?*
Carcinomas (90% of cancers, but epithelial cancers) - Squamous cell carcinoma - Transitional cell carcinoma - Adenocarcinoma (glandular) - Basal cell carcinoma (skin)
42
What are the benign and malignant connective tissue neoplasms called?*** TABLE ON SLIDE 37
- Leiomyoma (smooth muscle) - Fibroma (fibrous tissue) - Bone (osteoma) - Chondroma (cartilage - Lipoma (fat) - Neuroma (nerve) - Neurofibroma (nerve sheath) - Glioma - malignant glioma if malignant Malignant = SARCOMA IF CONNECTIVE TISSUE
43
What are germ cell neoplasms called?
Testis: Malignant teratoma (always malignant in testicles) Seminoma ``` Ovary: Benign teratoma (99.9% benign) ```
44
What is the definition of invasion?
Breach of the basement membrane with progressive infiltration and destruction of the surrounding tissue
45
What is the definition of metastases?
Spread of tumour to sites that are physically discontinuous from the primary tumour
46
How do malignancies occur?*
1. Growth and invasion at the primary site 2. Entering a transport system to be carried to the secondary site, where the growth lodges 3. Colonisation of the secondary site to form a new tumour 4. Each of the metastases create their own metastases
47
What is needed for a carcinoma cell to invade a tissue?
- Altered adhesion - Stromal proteolysis - Motility Cell begins to look more like a stromal cell than an epithelial cell (EPITHELIAL TO MESENCHYMAL TRANSITION)
48
How do neoplasms spread to distant sites?
- Blood vessels: sarcoma typically, mainly veins - Lymphatic vessels - Fluid in body cavities (transcoelomic) - pleura, peritoneum, pericardium
49
How does a carcinoma cell adhere?
- Reduces E-cadherin expression (intercellular adhesion molecules, so less sticking to teach other) - Changes in integrin expression
50
What is stromal proteolysis?
- Altered expression of proteases from adjacent connective tissue (eg. metalloproteinases) - Able of making their own proteolytic enzymes - Degrade BM and stroma = invasion
51
How do malignant cells invade and metastasise?*
- Taking advantage of nearby non-neoplastic cells to provide them with growth factors and proteases?
52
How do cells move?
Changes in actin cytoskeleton
53
How do malignant cells colonise the secondary site?
Most lodge at secondary sites as tiny, clinically undetectable cell clusters that can die or grow into metastases
54
How can the spread of metastases be stopped?
Preventing colonisation/failed colonisation
55
What are micrometastases?
Surviving microscopic deposits that fail to grow
56
Why does angiogenesis occur?
- To allow blood flow to cells at the centre of the tumour to gain oxygen and not become hypoxic - Can spread by blood
57
What are the common sites of blood-borne metastases?
Lung, liver, bone, brain
58
Which cancers tend to spread through lymphatics first?
Carcinomas
59
Which common neoplasms can spread to bone?
- Breast - Bronchus - Kidney - Thyroid - Prostate
60
Why does prostate cancer cause osteosclerotic metastases?
Causes increased production of disorganised, abnormal bone
61
What are the majority of lesions caused by metastases?
Osteolytic: destruction of bone tissue
62
Why are people in remission rather than cured of cancer?
Unknown whether or not there are dormant micrometastases present.
63
What determines the site of a secondary tumour?
Regional blood drainage, lymph, caulomic fluid Lymphatic: draining lymph nodes Breast: ipsilateral axillary LN
64
How are metastases spread transcoelomically?
Through other areas in coelemic space/adjacent organs
65
What is the 'seed and soil' phenomenon?*
Unpredictable distribution of blood-borne metastases | - interaction between malignant cells and local tumour environment (needs a good environment)
66
What is GSM?*
Grade: differentiation Spread: spread of tumour Metastases: how many lymph nodes/distant organs are invaded
67
Which malignant neoplasms rarely metastasise?
Basal cell carcinoma
68
Which malignant neoplasm is very aggressive?
Small cell carcinoma of the bronchus - early widespread systemic metastases/very locally advanced
69
What is the immune response to tumours?
- Recognition by immune system as non-self - Destroyed (cell mediated) - Tumour antigens recognised by CD8+ cytotoxic T cells, so immunocompromised patients are also at higher risk
70
How can tumours avoid the immune system?
- Loss/reduced expression of histocompatibility agents - Expression of factors that suppress immune system - Failure to produce the tumour antigen
71
What are the indirect, systemic effects of neoplasms?
- Increased tumour burden = parasitic effect - Reduced appetite, weight loss, malaise, thrombosis - Production of hormones (usually by benign tumours)
72
What are the local effects of neoplasms?
- Direct invasion and destruction of normal tissue - Ulceration at surface - Compression of adjacent surfaces - Blocking tubes and orifices - Raised pressure due to growth
73
What are paraneoplastic syndormes?
Signs and symptoms that cannot be readily explained by the anatomic distribution of the tumour, or by the production of hormones from the tissue in which it arose (10% of patients)
74
Why are paraneoplastic syndromes important?
- Earliest manifestation of neoplasm? - Significant clinical problems and fatality - Mimicking metastatic disease
75
What causes hypercalcaemia in neoplastic disease?
- Osteolysis due to primary bone lesions due to myeloma/secondary mets - Production of calcaemic humoral substances by neoplasms outside of the bone (only then paraneoplastic)
76
What is cachexia?
Equal loss of fat AND muscle: patient presenting with anorexia, anaemia, reduced appetite
77
What are other paraneoplastic syndromes?
- Neuropathies (brain and peripheral nerves) - Skin problems (pruritus, abnormal pigmentation) - Fever - Finger clubbing - Myositis (muscle inflammation) - Cushing's syndrome (steroid production)

Pathological Processes (10 decks)

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