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Pathological Processes > Session 8 > Flashcards

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
Q

What is a monoclonal population?

A

A population that call came from the same single cell precursor

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26
Q

Why do people with genes get the cancers earlier?*

A

In germline mutations the neoplastic cells can miss out the steps of proliferation and then appear quicker

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27
Q

How does a neoplasm form from monoclonal cells?

A

Progression: accumulation of more mutations

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28
Q

What is progression?

A

Gaining more mutations that can give advantages (eg. autonomous growth to avoid checkpoints)

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29
Q

What genes are affected?

A
  • Genes regulating apoptosis
  • Genes involved in DNA repair
  • Growth inhibiting tumour suppressor genes
  • Growth promoting proto-oncogene
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30
Q

What are proto-oncogenes?

A

Genes with multiple functions that participate in signalling pathways driving proliferation

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31
Q

How do proto-oncogenes mutate?

A
  • 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
Q

Why is cancer so common?

A

Only one oncogene needs to be mutated as they are dominant over normal counterpart of the gene

33
Q

What is a tumour suppressor gene?

A

A gene that stops cell proliferation (tp53 more common; regulates cell cycle progression)
- Most frequently mutates

34
Q

How do tumour suppressor genes cause cancer?

A
  • Recessive (both alleles damaged)
  • Loss of function mutation
  • Failure of growth inhibition
35
Q

How do apoptosis regulating genes cause neoplasia?

A

Acquire abnormalities that result in less cell death and enhanced survival of cells with abnormalities

36
Q

What are DNA repair genes?

A

Genes that are able to recognise and repair non-lethal genetic damage in other genes

37
Q

How do DNA repair gene damages cause neoplasia?

A
  • Loss of function
    Direct contribution
  • Impair ability to recognise and repair the cells
  • Affected cells acquire more mutations more quickly
38
Q

What is a benign tumour called?

A
  • Usually ends with -oma
39
Q

What are epithelial neoplasms called?*

A
  • Stratified squamous: squamous papilloma (if fingerlike projections)
  • Transitional cell papilloma
  • Adenoma/cystadenoma
40
Q

What are the polyp names of benign neoplasms?*

A

Villous, sessile, tubular

41
Q

What are epithelial neoplasms called?*

A

Carcinomas (90% of cancers, but epithelial cancers)

  • Squamous cell carcinoma
  • Transitional cell carcinoma
  • Adenocarcinoma (glandular)
  • Basal cell carcinoma (skin)
42
Q

What are the benign and malignant connective tissue neoplasms called?***

TABLE ON SLIDE 37

A
  • 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
Q

What are germ cell neoplasms called?

A

Testis:
Malignant teratoma (always malignant in testicles)
Seminoma

Ovary: 
Benign teratoma (99.9% benign)
44
Q

What is the definition of invasion?

A

Breach of the basement membrane with progressive infiltration and destruction of the surrounding tissue

45
Q

What is the definition of metastases?

A

Spread of tumour to sites that are physically discontinuous from the primary tumour

46
Q

How do malignancies occur?*

A
  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
Q

What is needed for a carcinoma cell to invade a tissue?

A
  • Altered adhesion
  • Stromal proteolysis
  • Motility

Cell begins to look more like a stromal cell than an epithelial cell (EPITHELIAL TO MESENCHYMAL TRANSITION)

48
Q

How do neoplasms spread to distant sites?

A
  • Blood vessels: sarcoma typically, mainly veins
  • Lymphatic vessels
  • Fluid in body cavities (transcoelomic) - pleura, peritoneum, pericardium
49
Q

How does a carcinoma cell adhere?

A
  • Reduces E-cadherin expression (intercellular adhesion molecules, so less sticking to teach other)
  • Changes in integrin expression
50
Q

What is stromal proteolysis?

A
  • Altered expression of proteases from adjacent connective tissue (eg. metalloproteinases)
  • Able of making their own proteolytic enzymes
  • Degrade BM and stroma = invasion
51
Q

How do malignant cells invade and metastasise?*

A
  • Taking advantage of nearby non-neoplastic cells to provide them with growth factors and proteases?
52
Q

How do cells move?

A

Changes in actin cytoskeleton

53
Q

How do malignant cells colonise the secondary site?

A

Most lodge at secondary sites as tiny, clinically undetectable cell clusters that can die or grow into metastases

54
Q

How can the spread of metastases be stopped?

A

Preventing colonisation/failed colonisation

55
Q

What are micrometastases?

A

Surviving microscopic deposits that fail to grow

56
Q

Why does angiogenesis occur?

A
  • To allow blood flow to cells at the centre of the tumour to gain oxygen and not become hypoxic
  • Can spread by blood
57
Q

What are the common sites of blood-borne metastases?

A

Lung, liver, bone, brain

58
Q

Which cancers tend to spread through lymphatics first?

A

Carcinomas

59
Q

Which common neoplasms can spread to bone?

A
  • Breast
  • Bronchus
  • Kidney
  • Thyroid
  • Prostate
60
Q

Why does prostate cancer cause osteosclerotic metastases?

A

Causes increased production of disorganised, abnormal bone

61
Q

What are the majority of lesions caused by metastases?

A

Osteolytic: destruction of bone tissue

62
Q

Why are people in remission rather than cured of cancer?

A

Unknown whether or not there are dormant micrometastases present.

63
Q

What determines the site of a secondary tumour?

A

Regional blood drainage, lymph, caulomic fluid
Lymphatic: draining lymph nodes
Breast: ipsilateral axillary LN

64
Q

How are metastases spread transcoelomically?

A

Through other areas in coelemic space/adjacent organs

65
Q

What is the ‘seed and soil’ phenomenon?*

A

Unpredictable distribution of blood-borne metastases

- interaction between malignant cells and local tumour environment (needs a good environment)

66
Q

What is GSM?*

A

Grade: differentiation
Spread: spread of tumour
Metastases: how many lymph nodes/distant organs are invaded

67
Q

Which malignant neoplasms rarely metastasise?

A

Basal cell carcinoma

68
Q

Which malignant neoplasm is very aggressive?

A

Small cell carcinoma of the bronchus - early widespread systemic metastases/very locally advanced

69
Q

What is the immune response to tumours?

A
  • 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
Q

How can tumours avoid the immune system?

A
  • Loss/reduced expression of histocompatibility agents
  • Expression of factors that suppress immune system
  • Failure to produce the tumour antigen
71
Q

What are the indirect, systemic effects of neoplasms?

A
  • Increased tumour burden = parasitic effect
  • Reduced appetite, weight loss, malaise, thrombosis
  • Production of hormones (usually by benign tumours)
72
Q

What are the local effects of neoplasms?

A
  • Direct invasion and destruction of normal tissue
  • Ulceration at surface
  • Compression of adjacent surfaces
  • Blocking tubes and orifices
  • Raised pressure due to growth
73
Q

What are paraneoplastic syndormes?

A

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
Q

Why are paraneoplastic syndromes important?

A
  • Earliest manifestation of neoplasm?
  • Significant clinical problems and fatality
  • Mimicking metastatic disease
75
Q

What causes hypercalcaemia in neoplastic disease?

A
  • 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
Q

What is cachexia?

A

Equal loss of fat AND muscle: patient presenting with anorexia, anaemia, reduced appetite

77
Q

What are other paraneoplastic syndromes?

A
  • 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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