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General Pathology > Neoplasia > Flashcards

Neoplasia Flashcards

1
Q

What is a Neoplasm?

A

An abnormal mass of tissue, the growth of which exceeds and is uncoordinated with that of normal tissue, and persists in the same excessive manner after cessation of the stimuli which evoked the change.

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2
Q

What is the most common male and female cancer?

A

Male: Colon-rectum
Female: Breast

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3
Q

What is the difference between a cancer and a neoplasm?

A

Neoplasm/Tumour: Benign (usually curable/generally harmless) or malignant (cancerous) growth
Cancer: only malignant

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4
Q

What is the biological behaviour of a benign neoplasm?

A
  • Slow growth rate
  • No infiltration
  • No metastasis
  • High patient survival rates after successful surgical removal
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5
Q

What is the biological behaviour of a low-grade malignant/borderline neoplasm?

A
  • variable growth rate
  • locally infiltrative
  • low or no metastatic potential
  • intermediate patient survival rates; tendency for local recurrence after successful surgical removal
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6
Q

What is the biological behaviour of a malignant neoplasm?

A
  • rapid growth rate
  • infiltrative
  • metastasising
  • poor patient survival rates; tendency for local and distant recurrence (metastasis)
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7
Q

List 4 gross features of benign neoplasms

A
  1. Smooth surface with a fibrotic capsule
  2. Compressed surrounding tissues
  3. Small to large (sometimes very large)
  4. Unlikely to show necrosis
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8
Q

List 4 gross features of malignant neoplasms

A
  1. Irregular surface without encapsulation
  2. Destruction of surrounding tissues
  3. Small to large
  4. Can be associated with necrosis and haemorrhage
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9
Q

List 8 microscopic features of Benign Neoplasms

A
  1. Growth by compression of surrounding tissue
  2. Highly differentiated, resembles normal tissue of origin
  3. Cells similar to normal and resemble one another, presenting a uniform appearance
  4. Few mitosis, those present are normal
  5. Necrosis unusual; degenerative changes may be present
  6. Distant spread (metastasis) does not occur
  7. DNA content usually normal
  8. Karyotype usually normal
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10
Q

List 8 microscopic features of Malignant Neoplasms

A
  1. Growth by invasion of surrounding tissue
  2. Well or poorly differentiated, does not normal tissue of origin
  3. Enlarged hyperchromatic irregular nuclei with large nucleoli; marked variation in size and shape of cells (pleomorphism)
  4. Increased mitotic activity; abnormal, bizzare mitotic figures
  5. Necrosis and haemorrhage common
  6. Distant spread (metastasis) may occur
  7. DNA content of cells increased
  8. Aneuploidy, Polyploidy, Clonal genetic abnormalities
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11
Q

How is fibroadenoma of the breast presented macroscopically?

A

Palpable breast lump, freely movable benign neoplasm as it is well-encapsulated.
A result of dysregulated cell proliferation

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12
Q

How is advanced breast carcinoma of the breast presented macroscopically?

A
  • Fixed, ulcerating mass
  • Irregular surface (jagged edges) without encapsulation to infiltrate and destroy the surrounding tissues including the skin
  • Metastasis to surrounding lymph nodes, pectoral muscle
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13
Q

How is fibroadenoma of the breast presented microscopically?

A
  • Smooth fibrous capsule present (indicates an expansile non-infiltrative pattern of growth)
  • Lined by a basal/myoepithelial layer
  • Highly differentiated structure of ducts that resemble normal ducts
  • Uniform nuclei of the cells (normal in appearance)
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14
Q

How is advanced breast carcinoma of the breast presented microscopically?

A
  • Poorly formed, Haphazard appearance of malignant glands (poorly formed)
  • Scattered in infiltrative manner
  • Not bound by a basement membrane
  • Pleomorphism (Nuclei + cell vary in shape and size)

Cytologically abnormal

  • Hyperchromatic nuclei
  • High nuclear-to-cytoplasmic ratio
  • Irregular nuclear outline
  • Coarse clumped chromatin
  • Enlarged nucleoli
  • Abnormal mitoses
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15
Q

What are the 2 principles of histologically differentiating benign and malignant tumours

A
  1. Architecture

2. Cytology

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16
Q

What are satellite nodules?

A

Metastatic nodules from Melanoma (highly malignant cancer of the skin)

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17
Q

What is the likely primary site of metastatic carcinoma to the liver?

A

GIT

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18
Q

What are the common organs for distant metastasis?

A

Liver, Lungs, Bones

Due to vascular drainage to these organs (richly vascularised)

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19
Q

How does one tell a metastatic tumour from a primary tumour?

A

The common gross appearance of metastatic tumour is multiple tumour nodules of more or less equal sizes

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20
Q

Are metastatic tumour nodules that look grossly “circumscribed” mean they are encapsulated?

A

No :(

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21
Q

What is the metastatic tumour in the brain called?

A

Solitary brain metastasis

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22
Q

Is the primary tumour always clinically apparent when the metastatic tumour is clinically obvious?

A

No :(

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23
Q

How can Neoplasms be classified?

A
  1. Anatomical site (Organ)
  2. Histogenesis (Cell of origin)
  3. Behaviour (Benign, Intermediate/Borderline, Malignant)
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24
Q

What are the different possible histogenesis classification of neoplasms

A

Carcinoma: Malignant epithelial neoplasms
Adenoma: BENIGN neoplasms of glandular origin arising in endocrine organ
Adenocarcinoma: Malignant neoplasms of glandular origin arising in endocrine organ
Sarcoma: Malignant mesenchymal neoplasms
Leukemia: Malignant blood cell neoplasms
Wilm’s Tumour: Malignant mixed neoplasm arising from more than one cell type (one germ layer) - renal anlage
Teratoma: BENIGN or malignant neoplasm arising from more than one cell type (multiple germ layers)

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25
Q

Factors determining resemblance of neoplasm to parent tissue

A
  1. Tissue architecture
  2. Cell morphology
  3. Substances produced by cells
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26
Q

How do we determine if it is of squamous cell origin?

A

Production of keratin

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27
Q

How to tell if it is of glandular origin?

A

Production of mucins (Apical Vacuoles)

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28
Q

What kind of neoplasm is it if there is teeth/hair found in the ovaries?

A

Teratoma - arises from totipotential germ cells and hence can form all tissue types (ectodermal, mesodermal, endodermal origin)

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29
Q

What is cancer caused by?

A

Cancer is the stepwise accumulation of genetic changes caused by Chemicals, Radiant energy, Viruses and other oncogenic microbes.
Some people may have cancer predisposition (genetic or immunological) which accelerates this stepwise accumulation.

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30
Q

What is a Carcinogen?

A

Any substance, radiation, or microbe that promotes carcinogenesis, which is the formation of cancer. This may be due to the ability to damage the genome, or disruption of cellular metabolic processes

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31
Q

What is a genetic change/mutation?

A

Permanent alteration in teh DNA sequence such that the sequence differs from what is found in most people.
This can occur in the gene, or gene regulatory elements leading to dysregulated expression of genes.

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32
Q

What are the 3 types of mutations?

A
  1. Point mutations
  2. Copy number variation
  3. Chromosomal translocation/gene rearrangement
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33
Q

What are the 3 types of point mutations?

A
  1. Silent mutation: Base substitutions in the triplet codon that result in no change of the amino acid/amino acid functionality when the altered messenger mRNA is translated
  2. Missense: Substitution of a different amino acid in the resulting protein. This may have no effect (Conservative) or may render a protein non-functional (Non-conservative)
  3. Nonsense: Substitution that results in the appearnace of a stop codon where previously there was a codon specifying an amino acid. This premature stop codon results in the production of a shortened and likely nonfunctional protein.
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34
Q

What are copy number changes?

A

Duplications and deletions of chromosomal segments.

This can range from small deletions/insertions (1-50bp) to huge chromosomal aberrations.

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35
Q

What are chromosomal translocations?

A

Chromosomal breakage and reattachment resulting in abnormal rearrangements of chromosomes.
Eg. Burkitt’s Lymphoma (Excessive and dysregulated synthesis of Myc protein)

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36
Q

What is an activating mutation?

A

Mutation which causes the gene to become functionally activated independent of normal control mechanisms.

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37
Q

What is an inactivating mutation?

A

Mutation which results in the loss of the normal function of the gene.

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38
Q

What are some features of acquired gene mutations?

A
  • Most common cause of cancer
  • Occurs in non-gamete cell after the conception of the individual
  • Passed along only to daughter cells descended from that cell, and so are not present in all cells of the body
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39
Q

What are some features of germline gene mutations?

A
  • Rare
  • Occurs in a reproductive cell (sperm or egg)
  • Mutation incorporated into the DNA of every cell in the body
  • Heritable and can cause cancer family syndromes
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40
Q

What is the Adenomatous Polyposis Cell gene?

A

The APC gene provides instructions for making the APC protein, which plays a critical role in several cellular processes. The APC protein acts as a tumour suppressor, which means that it keeps cells from growing and dividing too fast or in an uncontrolled way. Hence, when there is mutation in the APC gene, cancer suppression is halted and the site is at risk of adenomas, which can then potentially become carcinomas (with homozygous loss of additional cancer suppressor genes, or overexpression of COX-2)

41
Q

What are the 6 hallmarks of cancer?

A
  1. Self-sufficiency in growth signals
  2. Evading Apoptosis
  3. Insensitivity to anti-growth signals
  4. Sustained angiogenesis
  5. Limitless replicative potential
  6. Tissue invasion and metastasis
42
Q

What are Proto-oncogenes?

A

Normal genes that are involved in promoting cell growth and proliferation. or inhibition of apoptosis

43
Q

What are Oncogenes?

A

Mutated Proto-oncogenes resulting in dysregulation and/or overexpression
Eg. c-myc

44
Q

What are Tumour Suppressor Genes?

A

Normal genes that negatively regulate cell proliferation, or stimulate apoptosis. They also repair DNA.
Any deletion or mutational inactivation will result in a loss of function and hence malignant transformation.
Eg. p53

45
Q

What are some environmental triggers of genetic changes?

A

Direct

  1. Chemical carcinogens (eg. alcohol, tobacco, smoking. betel nut chewing, asbestos)
  2. Radiant energy (eg. UV light, X-rays)

Indirect
3. Viruses (eg. Human Papillomavirus, Epstein-Barr virus, Hepatitis B virus, Hepatitis C virus)

46
Q

How do viruses cause cancer?

A
  1. Oncogenic effects of viral gene products that subvert normal function of cellular genes
  2. Integration of viral genome into host cell DNA
47
Q

What are the oncogenic effects of HPV E6 and E7?

A 
Inhibit p53 (tumour suppressor gene) hence blocking apoptosis.
E7 also inhibits p21 and RB-E2F which hence removes the restraints on cell proliferation.
48
Q

When do pre-malignant conditions arise?

A

When there is accumulation of sufficient genetic changes resulting in cellular and tissue alterations and damage

49
Q

What is the effect of cancer predisposition (genetic, immunological)

A

It may lead to early development of the pre-malignant state or multiple lesions.

50
Q

What are some examples of suspicious lesions that might be biopsied to assess for pre-malignancy?

A
  1. Squamous lesions
  2. Glandular lesions
  3. Many chronic inflammatory lesions eg. Chronic peptic ulcer, Ulcerative colitis
51
Q

What is example of an inheritable cancer predisposition syndrome?

A

Familial Adenomatous Polyposis (FAP)
It is the most common polyposis syndrome.
Caused by mutation of the Adenomatous Polyposis Cell (APC) gene - Autosomal dominant inheritance
Causes development of large numbers of colonic adenomas with glandular dysplasia that usually develops into carcinoma.
Treatment: Prophylactic total colectomy

52
Q

What are some oral manifestations of Familial Adenomatous Polyposis (FAP)?

A 
Supernumerary teeth
Congenitally missing teeth
Odontomas
Dentigerous cysts
Fused molar roots
53
Q

What is Gardner’s Syndrome?

A

A variant of Familial Adenomatous Polyposis (FAP) where tooth extraction is very difficult (due to dense nature of alveolar bone and hypercementosis hence causing absence of peridontal space)

54
Q

What are the microscopic features of Epithelial Dysplasia?

A
  • Loss of architectural order
  • Loss of maturation
  • Loss of uniformity of individual cells
  • Nuclear pleomorphism
  • Increased mitotic activity
55
Q

What are the 4 grades of squamous dysplasia?

A
  1. Normal
  2. Hyperplasia - benign, reactive, will reverse if noxious stimuli is removed
  3. Mild/moderate dysplasia
  4. Severe dysplasia
56
Q

Must dysplasia be treated?

A

Mild dysplasia need not be treated but need to be closely monitored.
Severe dysplasia should be treated as it has a high risk of developing invasive carcinoma.

57
Q

What is the difference between severe epithelial dysplasia and epithelial carcinoma?

A

Severe epithelial dysplasia has the cytological hallmarks of malignant epithelial cells, BUT have not developed the ability to penetrate through the basement membrane. Carcinoma is invasive and hence can penetrate through the basement membrane.

58
Q

What are the different grades of cervical intra-epithelial neoplasia (CIN)?

A

CIN I to III
They have gradual loss of surface maturation.
Increase grade = Increase severity

59
Q

How can one detect to prevent cervical cancer?

A

Papanicolaou smears to detect the presence of dysplastic cells

60
Q

What is Anti-tumour immunity?

A

T cells from our immune system carry out cancer immunosurveillance to recognise tumour antigens, become activated and kill tumour cells. Hence, there is increased incidence of malignancies in immunosuppressed individuals.

61
Q

How do tumours evade the immune system?

A

Established tumours can create an immunosuppressive tumour micro-environment to evade anti-tumour immune responses.

Lack of T cell recognition of tumour

  1. Antigen-loss variant of tumour cell
  2. Mutations in MHC genes or genes needed for antigen processing

Inhibition of T cell activation

  1. Production of immunosuppressive proteins (eg. immunosuppressive cytokines)
  2. Expression of inhibitory cell surface proteins
62
Q

What cancer does Epstein Barr Virus increase susceptibility to?

A

Lymphoma

63
Q

What cancer does Human Herpes Virus 8 increase susceptibility to?

A

Karposi Sarcoma, Lymphoma

64
Q

How do tumours exploit PD-1 dependent immune suppression for immune evasion?

A
  1. Tumour antigens are recognised by Tumour-Infiltrating Lymphocytes (TIL)
  2. There is PD-L1 induction onto tumour site by IFNy
  3. PD-L1 on the tumour site engages with PD-1 on TILs
  4. TIL is deactivated/undergoes dysfunction
65
Q

How can the anti-tumour function of Tumour Infiltrating Lymphocytes (TIL) be augmentated

A

By blocking PD-1/PD-L1 interactions with monoclonal antibodies

66
Q

What cancers should one undergo early screening and detection for?

A 
Breast
Cervix
Stomach
Colon
Members of cancer families
67
Q

For whom is screening for cancers especially important for?

A

Those who have high-risk occupations which are exposed to carcinogens

68
Q

How can cancer be prevented?

A
  1. Early Screening
  2. Occupational Health Services
  3. Legislating Exposure Limits
  4. Public Education of carcinogens
  5. Vaccination
69
Q

Why is grading and staging of malignancies important?

A

This is to predict the clinical behaviour of a malignant tumour and to establish the criteria for therapy (decide on the appropriate therapeutic regimen and compare the efficacy of different therapeutic regimens)

70
Q

What is the grade of a malignant neoplasm?

A

The degree of malignancy determined by the degree of differentiation (morphologically and functionally). It is determined HISTOLOGICALLY

71
Q

What are the grades of Malignant Neoplasms

A

Grade 1: Well Differentiated
Grade 2: Moderately Differentiated
Grade 3: Poorly Differentiated

Some grading systems have 2/4 grades.

72
Q

What are some cytologic evidences of anaplasia/cytologic atypia?

A
  1. Variation in size and shape of cells
  2. Variation in size and shape of nuclei
  3. Enlarged and hyperchromatic nuclei
  4. High Nuclei to cytoplasm ratio
  5. Clumped chromatin
  6. Prominent Nucleoli
  7. Atypical Mitosis
  8. Bizarre Cells
73
Q

How are cancers disseminated?

A
  1. Local Infiltration
    a. Perineural Infiltration (infiltrate into area surrounding nerves)
    b. Pagetoid Spread (along epidermis and epithelial linings)
  2. Spread through body cavities
  3. Lymphatic Spread
  4. Hematogenous Spread
74
Q

Do all malignant tumours have irregular borders>

A

No. Some slowly expanding malignant tumours can have a deceptively well demarcated appearance as their pattern of growth is by pushing along a broad front.

75
Q

What is emphasised in cancer surgery?

A

That the cancer is completely removed and resection margins are clear of tumour involvement. If not there will definitely be tumour recurrence.

76
Q

What type of dissemination is a spread to adjoining organs?

A

Local infiltration.
Eg. rectal cancer can grow and infiltrate the wall and involve the bladder; squamous cell carcinoma of the oral mucosa can infiltrate through the soft tissue to involve the mandible or maxilla

77
Q

Where is Perineural Infiltration seen in?

A

Head and Neck Tumours

78
Q

Why are Perineural Infiltrated tumours difficult to completely resect?

A

This is because they spread microscopically around nerves.

79
Q

What is the common symptom resulting from tumour infiltrating the perineural space?

A

Pain >.

80
Q

What is an example of Pagetoid Spread?

A

Paget Disease of the nipple (1-4% of breast cancer)
It presents as a unilateral erythematous eruption with a scale crust. Pruritus (itchiness) is common). The malignant cells creap up the breast ducts into the lactiferous sinus and into the nipple skin without crossing the basement membrane.

Large cancer cells are scattered within the epidermis

81
Q

What prognosis does seeding of body cavities dissemination of cancer have?

A

A bad prognosis. This is because the tumour has penetrated a natural “open field”. It is also inoperable. and is not uncommonly seen in late stages of cancers of the GIT and ovarian cancers.

82
Q

What cavities are involved in the seeding of body cavities?

A

Peritoneal cavity (Clinically presents and Ascites - abnormal build up of fluid in the abdomen)
Pleural Cavity (Clinically presents as Pleural Effusion and can cause respiratory compromise)
Pericardial Cavvity
Subarachnoid
Joint Spaces

83
Q

What is Krukenberg Tumour?

A

Metastatic Carcinoma involving bilateral ovaries arising from a primary in the stomach spread by the peritoneal cavity

84
Q

What type of biopsy is performed regularly for breast carcinomas?

A

Sentinel node biopsy. This is to check for lymph node involvement following the natural route of lymphatic drainage to check for dissemination of cancer via lymphatic spread.

85
Q

Does an enlarged regional lymph node mean there is metastatic spread?

A

Not necessarily! It could just be due to reactive hyperplasia

86
Q

Where do head and neck cancers usually metastasise to?

A

Cervical Lymph Nodes

87
Q

What are the 2 haemotogenous spread systems?

A
  1. Portal Venous Drainage System (GIT to Liver)

2. Caval Venous Drainage System (Body to Lungs)

88
Q

How are vertebral columns usually involved in cancers?

A

Through metastasis of cancers in close proximity to the vertebral column (prostate/thyroid) embolising through the paravertebral venous plexus (haemotogenous spread)

89
Q

What is staging of cancers for?

A

To assess how extensively the primary lesion has grown + extent of spread to regional lymph nodes + presence/absence of blood borne metastasis

90
Q

What does the TNM cancer staging system stand for?

A

T - Tumour in primary site
N - Lymph nodes, Regional
M - Distant metastasis

Within each letter element, increasing involvement is categorised by the combination of the capital letter with a numerical suffix.

TNM system for cancers in different organs are different.

91
Q

What does TX stand for?

A

Primary tumour cannot be assessed (may be prior to assessment)

92
Q

What does T0 stand for?

A

No evidence of primary tumour

93
Q

What is the process of tumour invasion?

A
  1. Intraepithelial
  2. Lamina Propria
  3. Submucosa
  4. Muscularis Propria
  5. Subserosa
94
Q

What are the local effects of tumour?

A
  1. Mass
  2. Ulcer (non-healing) - epithelial surfaces
  3. Haemorrhage - vessels
  4. Pain - sensory nerves
  5. Seizures - brain
  6. Obstruction eg. pneumonia (bronchial), jaundice (bile ducts)
  7. Perforation
  8. Bone destruction
  9. Inflammation
  10. Space-occupying lesion
  11. Cerebral Dysfunction
  12. Localised loss of sensory or motor function - nerve or nerve trunk
  13. Oedema - venous/lymphatic
95
Q

Can benign lesions cause death?

A

Yes
Due to
1. Site eg. Meningioma (increased intracranial pressure); Teratoma in the ovaries (infarction due to blockage of blood vessels)
2. Function eg. Insulinoma (produces insulin hence causing hypoglycemia); Parathyroid neoplasms (produces PTH resulting in many complications eg. Hypercalcaemia)

96
Q

What are paraneoplastic syndromes?

A

Symptom complexes in cancer patients not attributable to local or distant spread of the tumour or hormonal effects indigenous to the tissue from which the tumour arose.
Eg. Cushing syndrome (ACTH), Inappropriate ADH secretion, Hypercalcemia (PTH)

97
Q

What are tumour markers?

A

Protein markers which are biochemical assays of isoenzymes, hormones, oncofoetal antigens, specific proteins eg. immunoglobulins and Prostate Specific Antigen (PSA), mucins and other glycoproteins

98
Q

Are tumour markers used for diagnosis of cancers?

A

No. They cannot be used for definitive diagnosis. Instead it is used as a screening method for detection + monitoring the amount of residual cancer + checking for tumour recurrence post therapy

99
Q

What are the functions of molecular markers?

A
  1. Predict response to therapy
  2. Monitor for tumour recurrence
  3. Prognostic markers of long-term survival

It is still an evolving area

General Pathology (10 decks)

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