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1.2.5. Pathological Processes > Neoplasia > Flashcards

Neoplasia Flashcards

1
Q

Define neoplasia

A

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

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2
Q

Define dysplasia

A

pre-neoplastic alteration in which cells show disordered tissue organisation.

It is not neoplastic = reversible - also represents altered differentiation.

Mild, moderate and severe dysplasia indicates worsening differentiation

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3
Q

Define tumour

A

clinically detectable lump/swelling

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4
Q

Define cancer

A

any malignant neoplasm

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5
Q

Define metastasis

A

malignant neoplasm that has spread from its original site to a new non-contiguous site

original location is the primary site and the place to which it has spread is a secondary site

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6
Q

Define anaplasia

A

Cells with no resemblance to any tissue

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7
Q

When a benign/malignant tissue is described as well differentiated, what does that mean?

A

Tissue that closely resembles the parent tissue

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8
Q

Define pleomorphism

A

increasing variation in size and shape of cells and nuclei

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9
Q

Define progression

A

The process of a neoplasm emerging from a monoclonal population, characterised by the accumulation of yet more mutations

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10
Q

Describe and compare benign and malignant tumours

A

Benign = confined to origin, pushing outer margin, rarely dangerous, do not metastasise.

Malignant = potential to metastasise, irregular outer margin/shape, may show areas of necrosis and ulceration (if on a surface)

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11
Q

What are the microscopic characteristics of neoplasms showing varying degrees of differentiation?

A

With worsening diff individual cells = increasing nuclear size and nuclear to cytoplasmic ratio,

increased nuclear staining (hyperchromasia),

more mitotic figures and increasing variation in size and shape of cells and nuclei

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12
Q

Define grade

A

Clinicians use the term grade to indicate differentiation, high grade being poorly differentiated

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13
Q

Distinguish between in-situ and invasive malignancy

A

In-situ = no invasion through epithelial basement membrane

Invasive = penetrated through basement membrane

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14
Q

What 3 factors enable a neoplasms to come about?

A

Initiators, mutations, promotors

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15
Q

Describe clonality of neoplasms

A

combination of initiators/promoters = expanded, monoclonal population of mutant cells.

Chemicals, infections, radiation = initiators but can also act as promoters.

Mutations can be inherited

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16
Q

What is lyonisation?

A

In early female embryogenesis one allele is randomly inactivated in each cell

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17
Q

What are proto-oncogenes?

A

Play normal role in cell signally for cell growth – when they change/mutate they remain always switched on

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18
Q

What are tumour suppressor genes?

A

Recessive (have to inactivate both alleles)

normally oppose/suppress neoplasm formation,

inhibiting cell cycle,

become inactive in cancer

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19
Q

What does the suffix –oma mean?

A

Benign neoplasm

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20
Q

Define carcinoma

A

Epithelial malignant neoplasm

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21
Q

Define sarcoma

A

Stromal malignant neoplasm

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22
Q

Define blastomas?

A

Formed from immature precursor cells

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23
Q

Where is squamous carcinoma found?

A

Squamous epithelial = skin larynx, oesophagus

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24
Q

What is adenocarcinoma?

A

Epithelial neoplasm of the glands

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25
Q

What is malignant melanoma?

A

Neoplasm of melanocytes or cells that devel from melanocytes

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26
Q

What is a teratoma?

A

Tumour composed of tissues not normally present – germ cell origin forms cell representing all 3 germ cell layer

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27
Q

What is Hodgkin’s lymphoma?

A

Type of lymphoma – with the presence of multinucleatedReed–Sternberg cells(RS cells) in lymph nodes

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28
Q

What does adenoma refer to?

A

Glandular

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29
Q

What is a papilloma?

A

Benign epithelial tumour growing exophytically (outwardly projecting)

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30
Q

Where is transitional cell carcinoma found?

A

transitional epithelial = bladder, ureters

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31
Q

What is a benign mesenchymal tumour?

A

Connective tissue neoplasm

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32
Q

What is a glioma?

A

Benign connective tissue neoplasm – in the brain/spine

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33
Q

Lymphomas

A

malignant neoplasms of lymphocytes, mainly affecting lymph nodes

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34
Q

What is a germ cell neoplasm?

A

arise from pluripotent cells, mainly in the testis or ovary

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35
Q

What is leukaemia?

A

neoplasm of blood-forming cells arising in the bone marrow

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36
Q

What is a myeloma?

A

Malignant neoplasm of plasma cells

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37
Q

What is a neuroendocrine tumours?

A

Arise from hormone secreting cells distributed throughout the body

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38
Q

Define invasion

A

Property of malignant neoplastic cells enabling them to infiltrate normal tissues and enter blood vessels/lymphatics

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39
Q

Outline the process that leads to metastasis

A

Grow/invade at primary site,

Enter a transport system and lodge at a secondary site,

Grow at the secondary site to form a new tumour (colonisation)

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40
Q

Invasion involves what 3 important alterations?

A

Altered adhesion, stromal proteolysis and motility

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41
Q

Explain epithelial-to-mesenchymal transition

A

Altered adhesion, stromal proteolysis and motility

= create a carcinoma cell phenotype that sometimes appears more like a mesenchymal cell than an epithelial cell

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42
Q

How is adhesion altered in carcinoma cells?

A

reduction in E-cadherin expression, changes in Integrin expression

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43
Q

How is stromal proteolysis altered in neoplasia?

A

cells must degrade basement membrane and stroma to invade

= altered expression of proteases, notably matrix metalloproteinases (MMPs)

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44
Q

How is motility altered in carcinoma cells?

A

changes in the actin cytoskeleton.

Signalling through integrins is important and occurs via small G proteins such as members of Rho family.

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45
Q

Describe the routes of metastases

A

Lymphatic,

blood: via capillaries and venules,
transcoelomic: fluid in body cavities (pleura, peritoneal, pericardial and brain ventricles)

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46
Q

What is a micrometastases?

A

Surviving microscopic deposits that fail to grow - apparently disease-free person may harbour many micrometastases, a phenomenon known as tumour dormancy

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47
Q

Outline what determines the site of metastases

A

1) where the regional drainage of blood (first capillary bed)/lymph (lymph node)/coelomic (elsewhere in coelomic space) fluid drain to.
2) seed and soil = interactions between malignant cells and local tumour environment (niche)

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48
Q

How do carcinoma spread vs sarcomas?

A

C = lymph. S = blood

49
Q

List the common sites of blood-borne metastases

A

Lung, bone, liver, brain

50
Q

List the neoplasms that most frequently spread to bone

A

Breast, bronchus, kidney, thyroid, prostate

51
Q

How can the effects of a neoplasm be broken down?

A

Local = Primary neo, secondary neo.

Systemic = burden, hormones, miscellaneous

52
Q

What is a paraneoplastic syndrome?

A

The systemic effects a neoplasm has on the body

53
Q

Which neoplasms commonly cause osteolytic lesions?

A

Osteosarcoma of the knee, breast/kidney/lung cancer metastasis

54
Q

which neoplasms commonly cause sclerotic lesions?

A

Prostate adenocarcinoma

55
Q

Describe the local effects of benign/malignant neoplasms

A

1) Direct invasion/destruction of normal tissue.
2) Ulceration at surface = bleeding.
3) Compression of adjacent structures.
4) Blocking tubes/orifices

56
Q

Describe the systemic effects of neoplasms

A

1) Endocrine: hormone prod by endocrine tumour, ectopic hormone prod.
2) Haematological: anaemia, thrombosis, DIC.
3) Neurological.
4) Dermatological.
5) General: cachexia, malaise, immunosuppression, fever, finger clubbing, hypercalcaemia, pruritis, myositis

57
Q

Discuss colorectal carinoma

A

predisposing = diet, obesity, smoking, lack of physical activity

pres = blood in the stool, a change in bowel movements, weight loss, lethargy

macroscopic = tumor growing outward

microscopic = irregular tubular structures, harboring pluristratification, multiple lumens, reduced stroma

staging = TNM

marker = over express cyclooxygenase-2 (COX-2) enzyme

screening = fecal occult blood testing, flexible sigmoidoscopy, and colonoscopy

58
Q

What is the presentation and appearance of osteosarcoma?

A

pres = bones pain

macroscopic = tumour on the bone

microscopic = neoplastic osteoblast

59
Q

What is the presentation and appearance of ovarian teratoma?

A

pres = pain/pressure in pelvis, irregular periods

macroscopic = contain hair, sebum, teeth

microscopic =tissue of all three germ layers

60
Q

What is the presentation of chronic lymphocytic leukaemia?

A

pres = enlarged lymph nodes , lethargy, breathless, hepatosplenomegaly

61
Q

What is the presentation and appearance of uterine leiomyoma?

A

Benign tumours from overgrowth of SM and CT in the uterus

pres = excessive menstrual bleeding (menorrhagia), anemia, infertility

macroscopic = multiple tumours

microscopic = spindle cells

62
Q

What is the most frequent cancer in men/women?

A

prostate/breast

63
Q

What are the 2 most common oesophagal tumours?

A

squamous cell carcinoma

adenocarcinoma

64
Q

What is an exophytic tumour?

A

grows out from the surface

common in benign neoplasms, indicated non-invasive

65
Q

What is a papillary tumour?

A

finger like projections

66
Q

What is a polypoid tumour?

A

exophytic mass often on a stalk

67
Q

What is a sessile tumour?

A

raised by flat

68
Q

What is an annular tumour?

A

encircling like a ring

69
Q

What is an endophytic tumour

A

invasion into surrounding tissue, irregular tumour margin

70
Q

When is tumour necrosis seen?

A

when the tumour grows rapidly and out-strips its blood supply

usually a feature of malignant tumours

71
Q

What is a lipoma?

A

benign neoplasm of adipose tissue

72
Q

What is kaposi’s sarcoma?

A

vascular neoplasm caused by human herpes virus 8 (HHV8)

usually in HIV +ve

73
Q

What does carcinogenesis mean?

A

causes of cancer

74
Q

Explain the multifactorial nature of neoplasia pathogenesis

A

Intrinsic = hereditary, age, gender, hormonal

extrinsic = environment, behaviour, lifestyle

75
Q

Explain how migration studies illustrate the relative contribution of intrinsic and extrinsic factors

A

Japanese-USA migration studies show 85% cancer risk extrinsic

76
Q

Outline extrinsic carcinogenic agents and their mechanisms of action

A

Chemicals = polycyclic hydrocarbons, aromatic amines, e.g., 2-naphylamine, nitrosamines

Radiation = UV and ionising

Infections = HPV, Epstein Barr virus, hep B/C, HIV, Helicobacter pylori, parasites

77
Q

What are pro-carcinogens?

A

Chems converted to carcinogens by CP450

78
Q

How is HIV carcinogenic?

A

acts indirectly by lowering immunity and allowing other potentially carcinogenic infections to occur

79
Q

How is HPV carcinogenic?

A

direct carcinogen because it expresses the E6 and E7 proteins that inhibit p53 and RB protein function respectively, both of which are important in cell proliferation.

80
Q

How is hepatitis carcinogenic?

A

indirect carcinogens that cause chronic liver cell injury and regeneration

81
Q

The functions of proto-oncogenes

A

Abnormally activated versions of normal genes that enhance neoplastic growth

82
Q

What is a tumour suppressor gene?

A

Inhibit neoplastic growth

Both alleles inactivated in neoplasia

83
Q

What is the role of RAS?

A

Proto-oncogene

Encodes G protein that pushes cell past cell restriction point

84
Q

What is the role of c-myc?

A

Transcription factors

85
Q

What is the role of c-erbB-2 (HER-2)?

A

Growth factor receptor

86
Q

What is the role of RB protein?

A

Major cell-cycle checkpoint = inhibit free entry in

Inactivation in both alleles in neoplasia

87
Q

What is the role of p53?

A

Role in inducing apoptosis

88
Q

What are caretaker genes?

A

Genes that maintain genetic stability

89
Q

What is the inheritance of Hereditary non-polyposis colon cancer syndrome?

A

Autosomal dominant

germline mutation affects one of several DNA mismatch repair genes

90
Q

What is the inheritance of Familial breast cancer?

A

Associated with BRCA1 BRCA2 genes that are important for repairing dsDNA breaks

Mutations can be found in sporadic malignant neoplasms

91
Q

What is the inheritance Retinoblastoma and the two hit hypothesis?

A

Dominant

2 hit hypo = first hit was delivered through the germline and affected all cells in the body. The second hit was a somatic mutation

In contrast, sporadic retinoblastoma has no germline mutation and so requires both hits to be somatic mutations and to occur in the same cell

92
Q

What is the inheritance of Xeroderma pigmentosum?

A

Autosomal recessive

Mutation in one of the 7 genes that affect DNA nucleotide excision repair

= very sensitive to UV damage = skin cancer at young age

93
Q

What are the 3 stages in carcinogensis?

A

Initiation

Promotion

Progression

94
Q

Outline initiation

A

= mutagens

95
Q

Outline promotion

A

Cause prolonged proliferation

96
Q

Outline progression including the adenoma-carcinoma sequence

A

= accum of multiple mutations

illustrated by colon carcinoma, which usually starts as a colonic adenoma, from which arises a carcinoma

97
Q

What are the 6 hallmarks of cancer?

A

1) self-sufficiency in growth signals;
2) resistance to growth stop signals;
3) no limit on the number of times a cell can divide (cell immortalisation);
4) sustained ability to induce new blood vessels (angiogenesis);
5) resistance to apoptosis;
6) the ability to invade and produce metastases

98
Q

What is genetic instability?

A

When chromosome segregation during mitosis is abnormal in malignant cells

99
Q

How is asbestos exposure related to the devel of tumours?

A

Rock can be ground down to for fibers

Used for buildings

Fibers can crumble = carcinogenic = lodge in lung = mesothelioma

100
Q

Why does the dye industry have linked to the devel of malignancies?

A

Exposure to 2-napthylamine = carcinogen

Show long delay between exposure and malignant neoplasm onset

Showed risk depends on carcinogen dosage

101
Q

What are the conditions associated with an increased risk of malignancy?

A

UC

Cirrhosis

Hashimotos thyroiditis

Chronic atrophic gastritis

102
Q

What is the leading cause of cancer-related death?

A

Lung 22%

103
Q

What is the commonest type of cancer in adults?

A

Breast, prostate, lung, colon/rectum = carcinomas = 53%

104
Q

What is the commonest type of cancer in children?

A

<14 = leukaemia, CNS, lymphomas

105
Q

Describe what is meant by tumour stage and understand its significance

A

TNM staging translated into I, II, III, IV

Standardised across the world

106
Q

Understand the principals of TNM staging

A 
T = size of primary tumour (T1-4)
N = nodes mets (N0-3)
M = metastatic spread (M0-1)
107
Q

Outline the Ann Arbor

A

Staging for lymphoma
I = single node
II = 2 separate regions on one side of diaphragm
III = spread both ides of diaphragm
IV = diffuse involvement of one or more extra-lymphatic organs such as bone marrow/lung

108
Q

What is the Dukes’ staging systems

A 
Staging for colorectal carcinoma
A = not through bowel
B = invasion through bowel wall
C = involve lymph nodes
D = distant mets
109
Q

Describe what is meant by tumour grade and understand its significance

A

Used for squamous cell carcinoma and colorectal carcinoma

G1 = well-diff
G2 = moderately diff
G3 = poorly diff
G4 = undiff/anaplastic
110
Q

Briefly outline the Bloom Richardson grading system for breast carcinoma

A

Assesses tubule formation, nuclear variation, number of mitoses

111
Q

Describe the principles behind surgery as a treatments for cancer

A

Surgery = aim to de-bulk tumour

112
Q

Describe the principle of radiotherapy as a treatment for cancer

A

x-rays or other types of ionising radiation to kill rapidly dividing cells.

Ds-DNA breaks cause damaged chromosomes preventing M phase from completing. Given in fractionated doses

113
Q

Describe Chemo as a treatment for cancer

A

antimetabolites = mimics normal substrates in DNA replication

alkylating = cross link DNA, lead to apoptosis

Abx = inhib DNA topoisomerase needed for DNA synthesis

plant-derived = blocks microtubules assembly and mitotic spindle formation

114
Q

Describe hormone therapy as a treatment for cancer

A

preventing oestrogen binding in breast cancer, blocking androgens binding in prostate cancer

115
Q

Describe targeted molecular therapies as a treatment for cancer

A

drugs that block immune checkpoints, targeting chromosomal translocations

116
Q

What is adjuvant treatment?

A

Why used: given after surgical removal of primary tumour to eliminate subclinical disease

Clinical disease free but on the premise they have micro-mets

117
Q

What is neoadjuvant treatment?

A

why used: given to reduce size of primary tumour prior to surgical excision

In-operable to operable

118
Q

Describe the use of tumour markers in diagnosis and monitoring of disease

A

Useful for monitoring tumour burden

Hormones = human chorionic gonadotropin (HCG)

Oncofetal antigens = carcinoembryonic antigen (CEA), alpha fetoprotein (AFP)

Specific proteins = prostate specific antigen (PSA)

Mucins and glycoproteins = cancer antigen 125 (CA 125)

119
Q

Describe UK cancer screening programs

A

Aim = detect as early as possible when the chance of cure is highest

Problems = lead time bias, length bias (how long it takes for a growth to present), over diagnosis picking up benign but believing they are malignant)

E.g. Cervix, breast, colorectal

1.2.5. Pathological Processes (11 decks)

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