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AA-Bloc A - Molecules to global health > Pathology - Neoplasia 1-2-3 > Flashcards

Pathology - Neoplasia 1-2-3 Flashcards

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Organic Chemistry 101 flashcards
1
Q

definition of a Lesion

A

Modification of tissue or organ due to an injury or disease process, often resulting in impairment of normal function

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2
Q

Is a tumor a neoplasm?

A

Yes

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3
Q

Is a mass, lump, a neoplasm?

A

No, its an aggregation of quantity of solid tissue

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4
Q

Definition of a Nodule

A

small rounded mass

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5
Q

Definition of a polyp

A

Any lesion or mass of tissue protuding from normal surface level, usually in lumen of a hallow organ

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6
Q

definition of a papilla (microscopic term)

A

finger-like projection consisting of surface epithelium over core of connective tissue (villus style)

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7
Q

Definition of a cancer

A

Any malignant neoplasm

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8
Q

definition of oncology

A

study of neoplasms, malignancies (or a medical specialty)

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9
Q

Examples of non-neoplastic growths

A
  • Malformations
  • Repair, if excessive healing
  • hypertrophy
  • hyperplasia
  • metaplasia
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10
Q

Definition of a choristoma

A

a malformation, synonym of ectobic tissue

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11
Q

Definition of hyperplasia

A

increase in cell numer in response to a stimulus, can be physiological or pathological

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12
Q

When/how does hyperplasia occurs

A

in occurs in cells with the capacity to divide, mediated by hormones or growth factors

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13
Q

Examples of hyperplasia

A
  • Hyperplasia of epithelial cells in the female breast during pregnancy
  • Hyperplasia of hepatocytes to regenerate liver parenchyma after partial resection
  • Prostatic hyperplasia in older males from androgens
  • Endometrial hyperplasia in postmenopausal women receiving estrogens
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14
Q

Why is hyperplasia not neoplasia

A
  • Cells are genotypically and phenotypically normal
  • The organ involved is usually (but not always) diffusely enlarged, i.e., does not form a localized mass
  • The hyperplasia generally ends when the stimulus ends, i.e., is generally reversible
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15
Q

In what case hyperplasia may be a precursor of neoplasia, example

A

endometrial hyperplasia may become endometrial carcinoma

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16
Q

Definition of metaplasia

A

replacement of one type of normall adult cell/tissue by another normal tissue.

It happens in epithelial tissues often mediated by inflammation

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17
Q

Examples of metaplasia

A
  • squamous metaplasia in bronchial epithelium due to smoking
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18
Q

definition of a neoplasm

A

A new (neo) growth or formation (plasma). A pathological disturbance of growth characterized by an excessive and unceasing proliferation of cells. Independant of normal regulatory control.

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19
Q

From what arise neoplasms and cancers

A

from DNA-related alterations passed to progeny cells (i.e. heritable), with added epigenetic changes

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20
Q

How are neoplasms classified?

A
  • organ or precise site
  • histological type
  • additional subtyping includes immunohistochemical, molecular, and genetic features
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21
Q

how do we call a malignant neoplasm on a squamous epithelium?

A

squamous cell carcinoma

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22
Q

malignant neoplasm on melanocytes

A

melanoma

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23
Q

malignant neoplasm in germ cells

A

dysgerminoma

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24
Q

benign melanocytes neoplasm

A

nevus

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25
Q

benign germ cells neoplasm

A

benign cystic teratoma

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26
Q

benign epithelial neoplasm

A

squamous papilloma

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27
Q

malignant fibroblasts neoplasm

A

fibrosarcoma

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28
Q

general name for malignant mesenchymal (solid tissue) neoplasm

A

Sarcoma

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29
Q

malignant adipocytes neoplasm

A

liposarcoma

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30
Q

malignant lymphoid cell neoplasm

A

lymphoma

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31
Q

malignant hematopoietic cells neoplasm

A

leukemia

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32
Q

malignant smooth muscle cells neoplasm

A

leiomyosarcoma

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33
Q

neoplasms are composed of:

A
  • the abnormal neoplastic cells with variable degrees of differentiation
  • a non-neoplastic stroma of connective tissue, inflammatory cells and blood vessels
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34
Q

name a liquid neoplasm

A

leukemia

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35
Q

macroscopy of a neoplasm

A
  • Mass, swelling, diffuse enlargement.
  • Circumscribed, to invasive and metastasizing (usually irregular shape)
  • Often pale or white

Secondary changes: ulceration, bleeding, necrosis

  • Invade, damage and destroy surrounding tissues, cause fractures…
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36
Q

malignant glandular neoplasm

A

adenocarcinoma

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37
Q

microscopic morphology of a neoplasm

A

abnormal cytology i.e. of individual cells or cellular atypia or pleomorphism: abnormal variation in cell size, shape, color, compared with normal ones in same tissue

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38
Q

possible change in the nucleus of a neoplasm

A

hyperchromasia, increased size and nucleo/cytoplasmic ratio, increased and abnormal mitoses (e.g., tripolar), more prominent nuclei

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39
Q

possible change in the cytoplasm of a neoplasm

A

tells us differentiation of cell type - loss of normal features, increased basophilia (more RNA)

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40
Q

how different is the histology of a neoplasm ?

A

Abnormal histoly because of dysorganization of the cells

  • loss of architecture, polarization
    -abnormal pattern, arrangement of the cells
  • invasion into surrounding tissues
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41
Q

what functional characteristics of the tissue of origin does a neoplasm retain?

A
  • cytoplasmic substances : keratin, mucin, bile
  • endocrine: production of hormones
  • innapropriate (ectopic) hormone secretion by non-endocrine neoplasms (e.g. with lung carcinoma)
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42
Q

Benign vs Malignant in terms of systemic effects

A

benign does not have a systemic effetcs, and malignant yes. potential for metastases

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43
Q

Is a malignant neoplasm encapsulated?

A

No, but benign yes.

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44
Q

benign glandular neoplasm

A

adenoma

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45
Q

local symptoms/signs of a benign neoplasm

A

obstruction, pressure, pain

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46
Q

complications of a benign neoplasm

A

bleeding, necrosis, ulceration, perforation. potential for malgnant transformation in some

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47
Q

2 main characteristics of malignant neoplasms

A
  • invasion : the ability to infiltrate and destroy surrounding tissues
  • metastatic potential : the ability to develop secondary foci (or metastases) of tumor growth at a distance from the primary tumor
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48
Q

How to make a diagnosis of malignancy?

A
  • clinical assessment
  • Macroscopic findings: imaging, pathologic assessment, and especially
  • microscopic evaluation (biopsy): marked cellular atypia, loss of architecture, invasion of surrounding tissues
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49
Q

what is the suffix for neoplasm

A

“oma”

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50
Q

name some caveats concerning benign and malignant neoplasm

A
  • Tumors of borderline or
    intermediate malignancy
  • Continuum between benign and malignant neoplasms
  • Special case of CNS neoplasms (can kill even if benign by increased intracranial pressure)
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51
Q

incidence of sarcomas vs carcinomas

A

carcinomas: more common
Sarcomas: less common

52
Q

etiology of carcinomas vs sarcomas

A

carcninomas: Generally known: environmental, viral

Sarcomas: viral, unknown

53
Q

Metastatic spread carcinomas vs sarcomas

A

carcinoma: lymphatics, then hematogenous

sarcomas: hematogenous

54
Q

Macroscopy difference carcinoma vs sarcomas

A

carcinoma: variably hard
Sarcoma: fleshy, firm

55
Q

Histological difference carcinoma vs sarcoma

A

carcinoma: from islands of cells separated by stroma
Sarcoma: sheets of spindle cells admixed with stroma between cells

56
Q

Histochemestry difference carcinoma vs sarcoma

A

carcinoma: epithelial e.g. mucin
Sarcoma: mesenchymal, e.g. fat

57
Q

immuno-histochemistry carcinoma vs sarcomas

A

carcinoma: Keratins
Sarcoma: vimentin, muscle actin (?)

58
Q

5 phases of biology of malignant neoplasm

A
  1. Transformation
  2. Growth - proliferation of transformed cells
  3. Diversification/clonal expansion of neoplastic cells
  4. local invasion
  5. Distant metastases
59
Q

What is transformation in the biology of malignancy?

A

process whereby normal cells become neoplastic or cancerous (carcinogenesis = oncogenesis=tumorigenesis)

60
Q

When/how does tranformation occurs in the biology of malignancy

A

occurs by the accumulation of genetic alterations and epigenetic changes so the cells can escape permanently from normal growth regulatory mechanism

61
Q

on what depends on how fast neoplastic cells double?

A

on the proliferation rate

62
Q

main cause of carcinoma of the cervix

A

HPV

63
Q

sequence of development of carcinoma of the cervix

A

normal -> dysplasia (or CIN I-II) -> carcinoma in-situ (or CIN III) -> invasive squamous cell carcinoma

CIN: Cervical intraepithelial neoplasia

64
Q

What are CIS

A

Carcinoma in situ : cells that are genotypically and phenotypically cancerous cells that remain localized to their tissue of origin, usually an epithelium

65
Q

why do we say that CIN are pre-malignant or pre-cancerous?

A
  • No invasion (yet) through the basement membrane (BM)
  • Because no lymphatics/blood vessels above BM, cannot metastasize

But it is NOT a benign neoplasm

66
Q

5 types of CIN and their associated intra epithelial grade

A

Condyloma = CIN I = LSIL
Mild dysplasie CIn I - LSIL
Moderate dysplasia = CIN II - HSIL
Severe dysplasia = CIN III - HSIL
CIS = CIN III = HSIL

67
Q

Other squamous/squamoid epithelia

A
  • Vaginal intraepithelial neoplasia, VIN
  • Skin, oral cavity, bronchus, laryns
  • urothelium (lining renal pelvis, ureters, bladder)
68
Q

What means “grading”

A

determination of degree of differentiation of a malignant neoplasm

69
Q

What is “differentiation”?

A

degree of resemblance to the normal/parent tissue

70
Q

What is de-differentiation?

A

loss of the ressemblance with normal tissue

71
Q

Anaplasia?

A

complete de-differentiation i.e. no resemblance to normal/parent tissue

72
Q

What means “low grade”

A

grade 1 = well differentiated = closest resemblance to parent tissue = better prognosis

73
Q

Squamous cell carcinoma grading

A
74
Q

what is meant by ‘‘levels of heterogeneity”

A

different histological types in one site - same histological type in different sites and subpopulations of cells in one neoplasm

75
Q

4 stages of the mechanism of invasion of CIS into underlying stroma to invasive carcinoma

A
76
Q

routes of metastases (3)

A
  1. lymphatic vessels to lymph nodes
  2. blood vessels (hematogenous)
  3. Transcoelomic (seeding via body cavities)
77
Q

Difference between staging and grading of malignant neoplasms?

A
  • staging is the determination of the size and extent of spread of a malignant neoplasm - has prognostic and therapeutic implication
78
Q

What is the TNM system?

A

-Primary tumor size, characteristics (T)
- presence or absence of lymph node metastases (N)
- Presence or absence of distant metastases (M)

79
Q

primary tool used for staging

A
  • resected surgical specimen (pathology) but also imaging, labs, etc.
80
Q

Tools to diagnose and stage neoplasms (6)

A
  • clinical (history, physical ex)
  • radiological/imaging
  • clinical laboratory (biochem, hemato)
  • tumor markers
  • Pathologic / tissue diagnosis (sytopatho, biopsy, histopatho)
  • Ancillary pathologic diagnosis techniques
81
Q

Examples of ancillary pathologic diagnosis techniques

A
  • immunohistochemistry :
    Diagnosis of histological type of malignancy
    Typing of lymphoma/leukemia (B, T-cell types…)
    Prognostic and predictive markers, e.g., estrogen, progesterone receptors
  • Flow cytometry
    Mostly for immunophenotyping of lymphomas/leukemias
  • Molecular/cytogenetic analyses
    Clonality of B or T-cell lymphomas
    Chromosomal alterations (mutations, deletions…)
    Prognostic and predictive indicator
82
Q

4 possible goals of therapy of neoplasms

A
  1. curative
  2. debulking
  3. adjuvant, neo-adjuvant
  4. Palliative
83
Q

possible therapies of neoplasms

A
  1. surgery
  2. radiation therapy
  3. chemotherapy
  4. immunotherapy
  5. targeted molecular therapies
84
Q

difference between prognostic and predictive factors

A

prognostic factors: determine outcome (chances of survival, 5-year survival rate)

Predictive factors: determine responsiveness of a neoplasm to a drug
(like the presence of certain proteins determines potential response to a drug)

85
Q

heritable factors account for higher proportion of some cancers, which one?

A

40% prostate
35% colo-rectum
25% breast

86
Q

what percentage of cancers are due to environmental, potentially avoidable causes?

A

80-90%

87
Q

Exogenous etiologies of cancer

A
  • chemical carcinogens
  • physical agents (radiation, uv)
  • biological agents (viruses, HPV, bacteria)
88
Q

Endogenous etiologies of cancer

A
  • Heredity
  • gender and hormones
  • altered immunity (age, immunosupressant drug, AIDS)
89
Q

Principle causes of human cancer

A

25% tobacco
25% diet
20% sexual behaviour, infection

90
Q

tobacco has a strong association with cancer of:

A

lung, mouth, pharynx, larynx, esophagus, pancreas, urothelium (kidney, bladder)

91
Q

what is the relative risk (RR) of a regular smoker vs passive smokers

A

regular RR 20
passive RR 1.15-1.2

92
Q

What is a direct-acting carcinogen

A

a chemical carcinogen that doesn’t need metabolic conversion

93
Q

What is a indirect-acting carcinogen

A

require metabolic conversion to mutagenic carcinogens

94
Q

what is a promotor in chemical carcinogenesis

A

not mutagenic, increase proliferation, including of cells with DNA mutations, favoring tumor growth (e.g., phorbol esters, hormones, alcohol…)

95
Q

how are classified carcinogens ?

A

in 3 groups
1. carcinogenic to human
2. probably/possibly carcinogenic
3. not classifiable as carcinogenic

96
Q

examples of medicinal drugs that are carcinogens

A
  • anti-cancer drugs
  • hormones like estrogens
  • immunosuppressants like cyclosporine
97
Q

examples of physical carcinogens

A
  • radiation : ionizinf x and beta rays, alpha beta particles (nuclear)
  • UV
  • elctromafnitic field (possibly carcinogenic) leukemia in children
98
Q

mechanism of UV as a carcinogen

A

formation of pyrimidine dimers, damaging DNA and overwhelming DNA repair mechanisms

99
Q

Mechanism of radiation as carcinogen

A

damage to chromosomes, translocations, mutations…

100
Q

link between chronic infections and cancer (may be)

A

Indirect via inflammation, cell damage and regeneration with ensuing proliferation (cf. promoters…) that allow the expression of new mutations

101
Q

Is HIV a direct or indirect carcinogen?

A

indirect - acts by its immunosuppressive effects

102
Q

Examples of direct carcinogen caused by an infection

A

HPV, EBV, HBV

103
Q

are bacteria/parasite a direct or indirect carcinogen?

A

indirectly, by cell damage, inflammation, cytokines

104
Q

difference between initiators and promoters

A

initiators (either direct or indirect acting, damaging DNA),
and promoters (increasing proliferation)

105
Q

characteristics of normal stem cells

A
  • Undifferentiated, capable of self-renewal
  • Asymmetrical replication
    One daughter cell differentiates → mature cell
  • Other daughter cell remainsan undifferentiated stem cell
106
Q

two main types of stem cells

A
  • embyonic, unlimited potential
  • adult stem cells
107
Q

possible use of stemm cell in regenerative medecine

A
  • Hematopoietic stem cells can be purified based on cell surface markers and used in stem cell transplantation to treat leukemias, lymphomas and some solid tumors
  • Embryonic stem cells used for in vitro fertilization
108
Q

characteristics of cancer stem cells

A
  • Capable of self-renewal, as normal stem cells
  • Potentially arise from transformation of
    Normal stem cells or Differentiated tissue cells
  • Must be eliminated to cure a cancer, but are resistant to therapy
109
Q

Why are cancer stem cells resistant to therapy

A
  • Low rate of replication, so less amenable to chemotherapeutic drugs that target rapidly dividing cells
  • Express factors such as multiple drug resistance 1 (MDR-1) that counter the effects of drugs
110
Q

to what can lead a molecular alterations of a cell ?

A

can be responsible for :
- transformation of a normal to a neoplastic cell,
- for its proliferation,
- continued growth,
- diversification and evasion of normal controlling mechanisms (e.g., apoptosis)

111
Q

how do you call multiple molecular alterations of a cell

A

multistep carcinogenesis

112
Q

most molecular alterations involve ___

A

DNA

113
Q

Driver vs Passenger (in mutation)

A

Driver: alter function of cancer genes, with direct control, clustered

Passenger: random, do not affect behavior, but may provide a selective advantage e.g., after therapy…

114
Q

hallmarks of cancer (resume card, high yield)

A
  • self-sufficiency in growth : unrestricted proliferation without external stimuli
  • insensitivity to growth inhibitory stimuli
  • altered cell metabolism
  • evasion of apoptosis
  • unlimited replicative potential
  • sustained angiogenesis (required in most0
  • invasion and metastasis
  • evasion of immune surevillance
  • Defects in DNA repair : genomic instability, facilitating mutations in protooncogenes and tumor supressor genes
115
Q

Primary effects of gene alterations in cancer:

A
  1. unrestricted proliferation without external stimuli, medicated by oncogenes, conferring self/sufficiency in growth signals
  2. insentivity to growth inhibitory stimuli : tumor suppressor genes, also resulting in unrestricted proliferation
  3. Defects in DNA repair genes: genomic instability, thereby facilitating mutations in proto-oncogenes and tumor suppressor genes
116
Q

Secondary gene alterations in cancer

A
  • Altered cellular metabolism
  • Evasion of cell death by apoptosis mediated by alterations intumor supressor genes or anti-apoptotic genes
  • Unlimited replicative potential: activation of telomerases (e.g., by mutated tumor suppressor genes )
  • Sustained angiogenesis required in most
  • Ability to invade and metastasize
117
Q

why do we need to know all the molecular stuff in oncology?

A

Because treatment will be designed according to what characteristic of cell alteration we face

e.g. cell sustaining proliferative signaling -> EGFR inhibitors

118
Q

what are oncogenes

A
  • are derevied from proto-oncogenes (normal genes involved in proliferation)
  • promote autonomous growth of cancer cells
119
Q

example of an oncogenes that present as a growth factor

A

platelet-derived growth factor (PDGF) secreted by glioblastomas and is a receptor on cell surface → autocrine loop (self stimulation)

  • cancer cells can make own growth factors to stimulate their own surface receptors, i.e., an autocrine loop (≠ normal paracrine loop)
120
Q

What can be oncogenes (5) ?

A
  • growth factor oncogene
  • growth factor receptors
  • signal transducing proteins
  • nuclear transcription factors
  • cycling and CDKs
121
Q

common oncogene that act as nuclear transcription factor

A

MYC, leads to Burkitt lymphoma

122
Q

What is the cell cycle?

A

the process a cell goes through to divide and make new cells

123
Q

How can cyclins and CDKs cause cancer?

A

mutations make cyclin or CDK overactive. it causes the cell to keep going through the cell cycle without stopping. This means the cancer cells keep dividing and growing uncontrollably.

124
Q

which gene is the guardian of the genome?

A

TP53

125
Q

What does wild P53 protein

A
  • Arrests cell cycle in late G1 via CDK inhibitor p21
  • Assists in DNA repair
  • Apoptosis if DNA cannot be repaired
  • Angiogenesis inhibitor via thrombospondin-1
126
Q

What does a MUTATED P53?

A

Genetic, Li-Fraumeni syndrome, SAs, leukemias, breast and adrenal cortical CAs

Somatic, homozygous, in breast, lung, colon CAs

AA-Bloc A - Molecules to global health (16 decks)

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