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pathoanatomy > neoplasia > Flashcards

neoplasia Flashcards

1
Q

definition of neoplasia

A

the uncontrolled, abnormal growth of cells or tissues in the body,

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2
Q

what are mesenchymal tumors?

A

tumors derived from the mesoderm, inculding bone, cartilage, fibrous tissue and other connective tissues

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3
Q

what is chondroma?

A

CARTILAGINOUS TUMOR. A benign tumor composed of cartilage, often found in the small bones of the hands and feet

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4
Q

what is a fribroma?

A

FIBROUS TUMOR. A benign tumor composed of fibrous or connective tissue, commonly found in the skin and subcutaneous tissue

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5
Q

what is an osteoma?

A

BONE TUMOR. A benign bone tumor, frequently occurring the bones of the skull and face

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6
Q

what are epithelial tumors?

A

tumors arising from epithelial cells, which originate from the ectoderm or endoderm.

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7
Q

what is an adenoma?

A

a benign tumor that forms in the glandular structures of epithelial tissue

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8
Q

what is a papilloma?

A

a benign tumor with finger-like projections, commonly found on the skin and in mucous membranes

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9
Q

what is a papillary cystadenoma?

A

a benign tumor that is both papillary and cystic, forming in glandular tissue, often found in the ovaries and pancreas

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10
Q

what is a polyp?

A

a growth projecting from a mucosal surface, commonly found in the colon, stomach, nasal cavity, and uterus.

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11
Q

list the different types of sarcomas?

A
  1. chondrosarcoma: cartilaginous tumor
  2. fibrosarcoma: fibrous tumor
  3. osteosarcoma: bone tumor
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12
Q

list carcinomas

A
  1. adenocarcinoma: gland forming tumor
  2. squamous cell carcinoma: squamous differentiation
  3. undifferentiated carcinoma: no differentiation
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13
Q

from which germ layers can carcinomas arise?

A

ectoderm, endoderm, and less likely, mesoderm

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14
Q

what is a well-differentiated neoplasm?

A

a neoplasm that resembles the mature cells of the cells of the tissue of origin

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15
Q

what is a poorly differentiated neoplasm?

A

a neoplasm composed of primitive cells with little differentiation

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16
Q

how is the biological behavior of an undifferentiated tumor usually characterized?

A

it often correlates with more aggressive and malignant behavior

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17
Q

what is the typical differentiation status of benign tumors?

A

well differentiated

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18
Q

how does the differentiation status of a tumor relate to its prognosis?

A

poorly differentiated malignant tumors usually have a worse prognosis than well-differentiated malignant tumors

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19
Q

what does dysplasia literally mean?

A

abnormal growth

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20
Q

what is malignant transformation?

A

a multistep process where normal cells become cancerous

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21
Q

what features are present in dysplasia?

A

some but not all of the features of malignancy are present, microscopically

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22
Q

can dysplasia develop into malignancy?

A

yes

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23
Q

Give examples of where dysplasia may develop into malignancy.

A

In the uterine cervix and colon polyps

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24
Q

How is dysplasia graded?

A

As low-grade or high-grade

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25
Q

How is high-grade dysplasia often classified?

A

It is often classified with carcinoma in situ (CIS).

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26
Q

what is the local invasion in context of malignant tumors?

A

the ability of malignant tumors to infiltrate and destroy surrounding tissues

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27
Q

what is the significance of a capsule in tumors?

A

benign tumors are often encapsulates, whereas malignant tumors usually lack a well-defined capsule, aiding in local invasion

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28
Q

what role does the basement membrane play in tumor biology?

A

the basement membrane is a barrier that, when breached by tumor cells indicates invasion and malignancy

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29
Q

what is metastasis?

A

the spread of cancer cells from the primary site to distant organs or tissues, and it is an unequivocal sigh of malignancy

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30
Q

what does seeding of body cavities mean in terms of metastasis?

A

the spread of cancel cells into body cavities, such as the peritoneal, pleural, or pericardial cavities, leading to secondary tumor formation

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31
Q

How do tumors metastasize through the lymphatic system?

A

Cancer cells enter lymphatic vessels, travel through lymph nodes, and potentially establish secondary tumors in distant sites.

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32
Q

How does hematogenous spread occur in cancer?

A

Tumor cells invade blood vessels and are transported via the bloodstream to distant organs, often the liver and lungs.

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33
Q

What surgical procedure was historically used to address nodal metastasis in breast cancer?

A

The Halsted radical mastectomy

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34
Q

What is a sentinel node biopsy?

A

A procedure to identify and remove the first lymph node(s) to which cancer cells are likely to spread from a primary tumor

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35
Q

Why is the number of involved nodes important in cancer staging?

A

It is a key component of the TNM staging system, which helps determine the stage of cancer and influences prognosis and treatment.

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36
Q

How does nodal involvement affect the prognosis of breast cancer?

A

The extent of nodal involvement is directly related to the risk of recurrence and overall prognosis.

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37
Q

What is adjuvant chemotherapy?

A

Additional cancer treatment given after the primary treatment to lower the risk of the cancer returning

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38
Q

Rate of growth - benign tumor

A

Progressive but slow. Mitoses few and normal

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39
Q

Rate of growth - malignant tumor

A

Variable. Mitoses more frequent and may be abnormal

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40
Q

Differentiation - benign

A

Well differentiated

41
Q

Differentiation - malignant

A

Some degree of anaplasia

42
Q

LOCAL INVASION - benign

A

Cohesive growth. Capsule & BM not breached

43
Q

LOCAL INVASION - malignant

A

Poorly cohesive and infiltrative!

44
Q

Metastasis - benign

A

absent

45
Q

Metastasis - malignant

A

may occur

46
Q

how does sun exposure relate to melanoma incidence?

A

higher sun exposure leads to higher melanoma incidence

47
Q

What is the incidence of melanoma among different racial groups and body areas?

A

Blacks have a low incidence of melanoma, and normally pigmented areas like the areolae on white people also have low incidence.

48
Q

How does body mass affect cancer risk?

A

Being overweight increases the risk of cancer by approximately 50%.

49
Q

How does viral exposure contribute to cancer risk?

A

Certain viruses are linked to specific cancers, such as HPV with cervical cancer, HBV with liver cancer, and EBV with lymphoma.

50
Q

What is the relationship between age and cancer incidence?

A

Most cancers occur in persons aged 55 years or older.

51
Q

What are common cancers in children?

A

Childhood cancers commonly include leukemias, CNS neoplasms, and bone tumors.

52
Q

What are characteristics of familial cancer syndromes?

A

Early age at onset, two or more primary relatives with the same cancer (soil theory), and the presence of multiple or bilateral tumors.

53
Q

What are nonhereditary predisposing conditions for cancer?

A

Conditions like chronic inflammation and precancerous states that increase the risk of developing cancer.

54
Q

What are examples of precancerous conditions?

A

Chronic ulcerative colitis, atrophic gastritis of pernicious anemia, and leukoplakia of mucous membranes.

55
Q

How does immune collapse relate to cancer risk?

A

Immune collapse, such as in immunodeficient states, can increase the risk of cancer by reducing the body’s ability to detect and destroy malignant cells.

56
Q

What initiates cancer at the molecular level?

A

Non-lethal genetic damage, which can lead to the transformation of normal cells into cancer cells.

57
Q
A
58
Q

How is a tumor formed?

A

A tumor is formed by the clonal expansion of a single precursor cell, resulting in a monoclonal population of cells

59
Q

What are the four classes of normal regulatory genes involved in cancer?

A

Proto-oncogenes, tumor suppressor genes, DNA repair genes, and apoptosis genes.

60
Q

What is carcinogenesis?

A

Carcinogenesis is a multistep process involving the accumulation of genetic and epigenetic alterations that ultimately lead to the transformation of normal cells into cancer cells.

61
Q

What are proto-oncogenes?

A

Normal cellular genes that regulate cell growth and differentiation, but when mutated or overexpressed, can become oncogenes and promote cancer developmen

62
Q

What are oncogenes, and what do they encode?

A

Oncogenes are mutated or overexpressed proto-oncogenes that encode oncoproteins, which promote uncontrolled cell growth and proliferation

63
Q

What do DNA repair genes do, and how are they involved in cancer?

A

DNA repair genes maintain the integrity of the genome by repairing damaged DNA; mutations in these genes can lead to genomic instability and cancer development

64
Q

What is the role of apoptosis genes in cancer?

A

Apoptosis genes regulate programmed cell death; mutations that disrupt apoptosis pathways can contribute to cancer by allowing abnormal cells to survive and proliferate.

65
Q

What determines the limited number of duplications a cell will undergo?

A

Telomeres, which are protective caps at the ends of chromosomes.

66
Q

What is the role of telomerase in cell replication?

A

Telomerase is an enzyme that adds repetitive nucleotide sequences to the ends of chromosomes, preventing telomeres from shortening with each cell division.

67
Q

How does telomerase affect the replicative potential of cells?

A

Telomerase, present in more than 90% of human cancers, changes telomeres so they will have unlimited replicative potential, enabling cancer cells to divide indefinitely.

68
Q

How close to a blood vessel must a cell be?

A

Approximately 1-2 mm.

69
Q

What signaling pathways are involved in the activation of angiogenesis?

A

Vascular endothelial growth factor (VEGF) and fibroblast growth factor-b (FGF-b).

70
Q

How is tumor size regulated?

A

Tumor size is regulated (allowed) by the balance between angiogenesis and anti-angiogenesis processes.

71
Q

What is angiogenesis?

A

Angiogenesis is the process of forming new blood vessels from pre-existing vessels, crucial for supplying nutrients and oxygen to growing tissues, including tumors.

72
Q

What is anti-angiogenesis?

A

Anti-angiogenesis refers to the inhibition or suppression of angiogenesis, which can be a therapeutic approach to limiting tumor growth by cutting off the blood supply to the tumor.

73
Q

What is the first step in tumor invasion?

A

Detachment, or “loosening up,” of the tumor cells from each other.

74
Q

What follows detachment in the process of tumor invasion?

A

Attachment of tumor cells to components of the extracellular matrix (ECM).

75
Q

How do tumor cells degrade the ECM?

A

Tumor cells secrete enzymes such as collagenase to degrade components of the ECM, facilitating invasion.

76
Q

What is the final step in tumor invasion?

A

Migration of tumor cells into surrounding tissues, facilitated by the changes in cell-cell and cell-matrix interactions.

77
Q

Where do translocations and inversions commonly occur?

A

In most lymphomas and leukemias, and increasingly in many non-hematologic malignancies as well.

78
Q

What is the initiation/promotion concept in carcinogenesis?

A

Both initiators and promoters are needed for cancer development, with neither being able to cause cancer independently.

79
Q

What do initiators (carcinogens) do in carcinogenesis?

A

Initiators cause mutations in DNA, which is the initial step in the development of cancer.

80
Q

How do promoters differ from initiators in carcinogenesis?

A

Promoters are not carcinogenic by themselves; they must take effect after initiation and enhance the proliferation of initiated cells.

81
Q

How do promoters contribute to carcinogenesis?

A

Promoters stimulate the proliferation of initiated cells, leading to the expansion of the mutated cell population and the development of cancer.

Flashcard 7

82
Q

What are some examples of chemicals that act as promoters in carcinogenesis?

A

Phenols, drugs, and various industrial chemicals can act as promoters in carcinogenesis.

83
Q

How do “initiated” cells respond to promoters?

A

“Initiated” cells, which have undergone genetic mutations predisposing them to cancer, respond and proliferate faster to promoters than normal cells, contributing to tumor growth and progression

84
Q

What is cachexia?

A

Cachexia is a complex metabolic syndrome characterized by severe weight loss, including both fat and muscle loss, often seen in advanced cancer patients.

85
Q

How does cachexia differ from simple reduced diet-induced weight loss?

A

Cachexia involves significant loss of both fat and muscle tissue, whereas reduced diet-induced weight loss primarily involves fat loss with preservation of muscle mass.

86
Q

What are some factors implicated in the development of cachexia?

A

Tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and Proteolysis Inducing Factor (PIF) are among the factors involved in the development of cachexia.

87
Q

How does TNF-α contribute to cachexia?

A

TNF-α is a pro-inflammatory cytokine that promotes muscle wasting and loss of appetite, contributing to the development of cachexia.

88
Q

What role does IL-6 play in cachexia?

A

IL-6 is another pro-inflammatory cytokine that is associated with muscle wasting and metabolic abnormalities seen in cachexia.

89
Q

What is PIF (Proteolysis Inducing Factor)?

A

PIF is a protein released by tumor cells that stimulates the breakdown of muscle proteins, leading to muscle wasting seen in cachexia.

90
Q

What are examples of nerve/muscle paraneoplastic syndromes?

A

Myasthenia gravis associated with thymoma or Lambert-Eaton myasthenic syndrome associated with small cell lung cancer are examples.

91
Q

What skin manifestations are associated with paraneoplastic syndromes?

A

Skin manifestations may include acanthosis nigricans or dermatomyositis, which can occur in association with underlying malignancies.

92
Q

What is HPOA (Hypertrophic Pulmonary Osteoarthropathy)?

A

HPOA is a paraneoplastic syndrome characterized by clubbing of the fingers and toes, periosteal new bone formation, and arthralgia, often associated with lung cancer.

93
Q

What vascular complications can occur in paraneoplastic syndromes?

A

Trousseau syndrome, which involves migratory thrombophlebitis, and nonbacterial thrombotic endocarditis are examples of vascular complications seen in some cancers.

94
Q

What hematologic manifestations can occur in paraneoplastic syndromes

A

Anemias

95
Q

How does nephrotic syndrome relate to paraneoplastic syndromes?

A

Some cancers can cause nephrotic syndrome through the production of circulating factors that affect the glomerular filtration barrier or through deposition of immune complexes in the kidney.

96
Q

What is grading in cancer?

A

Grading assesses the degree of cellular differentiation and the aggressiveness of the tumor,

97
Q

What is staging in cancer?

A

Staging evaluates the extent of the disease based on the size of the primary tumor, its involvement of nearby tissues or organs, and the presence or absence of metastasis to distant sites.

98
Q

What does the TNM system stand for?

A

Tumor, Node, Metastasis, and is widely used for staging various types of cancer.

pathoanatomy (7 decks)

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