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Rapid Review Pathology > Chapter 9 - Neoplasia > Flashcards

Chapter 9 - Neoplasia Flashcards

0
Q

What is the origin of squamous and transitional epithelium?

A

Ectoderm: squamous or transitional epithelium

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1
Q

Benign tumors: epithelial or connective tissue origin

A

Benign tumors: epithelial or connective tissue origin

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2
Q

What is the origin of glandular epithelium?

A

Endoderm: glandular epithelium

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3
Q

What is the origin of epithelium?

A

Epithelial origin: derive from ectoderm or endoderm

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4
Q

Connective tissue is derived from which embryonic tissue?

A

Connective tissue: mesoderm

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5
Q

What is a mixed tumor?

A

Mixed tumor: two patterns; same germ cell layer; e.g., parotid gland tumors

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6
Q

Teratomas can be derived from which germ cell layers?

A

Teratoma: ectoderm, endoderm, mesoderm

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7
Q

Where are teratomas located?

A

Teratomas: at or close to midline; ovary MC site

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8
Q

What are the sites for squamous cell carcinoma?

A

SCC sites: mouth, larynx, cervix

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9
Q

What are the sites for an adenocarcinoma?

A

Adenocarcinoma sites: distal esophagus → rectum; pancreas, breast, kidneys

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10
Q

What are the sites for a transitional cell carcinoma?

A

TCC sites: bladder, ureter, renal pelvis

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11
Q

What is the origin of sarcomas?

A

Sarcomas: connective tissue origin

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12
Q

What is a hamartoma?

A

Hamartoma: nonneoplastic overgrowth tissue; bronchial hamartoma

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13
Q

What is a choristoma? Give an example.

A

Choristoma: normal tissue foreign location; pancreatic tissue stomach wall

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14
Q

Define parenchyma.

A

Parenchyma: neoplastic component

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15
Q

Define stroma.

A

Stroma: nonneoplastic supporting tissue

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16
Q

What question describes the grade of a cancer?

A

Grade of cancer: does cancer resemble its parent tissue?

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17
Q

Give two examples of features of a low grade cancer.

A

Low grade: keratin pearls, glands with lumens

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18
Q

Describe a high grade cancer.

A

High grade/anaplastic: no differentiating features

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19
Q

How do cell organelles differ between a normal cell and a malignant cell?

A

Fewer mitochondria; less prominent RER; loss of cadherins

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20
Q

How do nuclear features differ between a normal cell and a malignant cell?

A

Both nucleus and nucleoli are larger with irregular borders

Malignant tumors: normal/abnormal mitotic spindles; hyperchromatic nuclei

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21
Q

Describe the metabolism of a malignant cell.

A

Malignant cells use anaerobic glycolysis for energy; ↑lactic acid in neoplastic cells

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22
Q

What is the role of PET scanning in cancer patients?

A

PET scan: diagnosis, staging, monitoring of therapy

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23
Q

What do malignant cells store in the cytosol?

A

Malignant cells store glycogen in the cytosol

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24
Q

Describe the growth rate of benign tumors.

A

Benign tumors have a slow growth rate

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25
Q

Describe the growth rate of malignant tumors.

A

Malignant tumors have a variable growth rate

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26
Q

What is the relationship between growth rate and the degree of differentiation?

A

Growth rate correlates with degree of differentiation

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27
Q

How many population doublings must occur in order for a tumor mass to become clinically detectable?

A

Clinically detectable: 30 population doublings to produce 10^9 cells (1 g tissue)

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28
Q

How are tumors with an increased growth rate treated?

A

Tumors with ↑growth rate treated with cell cycle–specific chemotherapy

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29
Q

What phases of the cell cycle are inhibited by methotrexate and vincristine?

A

Methotrexate inhibits S phase; vincristine inhibits M phase

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30
Q

Describe the origin of most benign and malignant tumors.

A

Most benign/malignant tumors arise from single precursor cell (monoclonal)

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31
Q

What are telomere complexes?

A

Telomere complexes: repetitive sequences nontranscribed DNA at ends of chromosomes

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32
Q

What is the function of telomere complexes?

A

Prevent end-to-end chromosome fusion during mitosis; important for cell longevity

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33
Q

What happens to telomeres with each cell division?

A

Telomeres shorten with each cell division; few nucleotide bases remain → signal for apoptosis

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34
Q

Describe the telomerase activity in malignant cells.

A

Malignant cells: telomerase activity upregulated; prevents apoptosis

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35
Q

What does upregulation of DAF prevent?

A

Upregulation DAF prevents MAC formation; cancer cells cannot be killed

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36
Q

Describe the properties of benign tumors with respect to invasion.

A

Benign tumors do not invade; enclosed by fibrous tissue capsule

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37
Q

What is the second most important criterion for malignancy?

A

Invasion: second most important criterion for malignancy

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38
Q

What tissues are resistant to invasion?

A

Tissues resistant to invasion: cartilage, elastic artery tissue

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39
Q

What is angiogenesis?

A

Angiogenesis: new capillary sprouts form from parent capillaries

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40
Q

Describe the role of TNF in angiogenesis.

A

TNF important in stimulating synthesis of angiogenesis factors

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41
Q

What does angiogenesis require?

A

Angiogenesis: requires growth factors, chemotactic factors, and enzymes

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42
Q

What from the bone marrow is also used in angiogenesis?

A

Angiogenesis also uses EPCs in producing new capillary sprouts

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43
Q

What does bevacizumab do?

A

Bevacizumab inhibits binding of VEGF to endothelial cells in new capillary sprouts

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44
Q

Within the primary tumor, what develops the capacity to invade and metastasize?

A

Clonal proliferation of cells can invade/metastasize

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45
Q

Describe the first step of invasion of malignant cells.

A

1st step invasion: lose cell-to-cell adhesion molecules (cadherins)

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46
Q

Describe the second step of invasion of malignant cells.

A

2nd step invasion: attach to basement membrane and degrade it

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47
Q

Describe the third step of invasion of malignant cells.

A

3rd step invasion: attach to ECM and degrade it

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48
Q

Describe the fourth step of invasion of malignant cells.

A

4th step invasion: stimulate cell motility

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49
Q

What is intravasation?

A

Invade capillaries to enter the circulation (intravasation)

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50
Q

What do malignant cells do while in the circulation?

A

Evade or be destroyed by host defense cells

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51
Q

What do malignant cells that successfully evade host defense cells do?

A

Form tumor emboli coated by fibrin and platelets

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52
Q

Where do tumor emboli attach? What subsequently occurs?

A

Tumor emboli attach to capillaries at target organ and repeat the 4-step process of invasion

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53
Q

Describe the homing of tumor cells.

A

Homing of tumor cells: chance deposition; Batson paravertebral plexus; produce chemokines that go to specific sites with chemokine receptors similar to primary tumor; chemoattractants released from target sites

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54
Q

What is the most important criterion of malignancy?

A

Metastasis most important criterion of malignancy

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55
Q

What criterion of malignancy is characteristic of basal cell carcinoma?

A

BCC invade but do not metastasize

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56
Q

Describe the first step for dissemination of carcinomas.

A

Carcinomas: lymphatic spread → regional nodes; first line of defense

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57
Q

Describe the hematogenous phase of cancer dissemination in carcinomas.

A

Tumor cells in nodes invade efferent lymphatics → systemic circulation

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58
Q

Describe the dissemination of sarcomas.

A

Sarcomas initially have hematogenous spread; avoid nodes

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59
Q

Where do malignant cells in the portal vein metastasize to?

A

Malignant cells in portal vein → metastasize to liver

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60
Q

Where do malignant cells in the vena cava metastasize to?

A

Malignant cells in vena cava → metastasize to lungs

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61
Q

What types of cancer have hematogenous spread?

A

Both carcinomas/sarcomas have hematogenous spread

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62
Q

Define seeding of malignant cells.

A

Seeding: exfoliation from serosal surface and invade tissue in body cavity

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63
Q

Give three examples of seeding of malignant cells.

A

Seeding: malignant surface-derived ovarian cancers; omental implants
Peripherally located lung adenocarcinomas seed pleural cavity
GBM uses spinal fluid to seed distant sites (brainstem, spinal cord)

64
Q

What is the most common site of bone metastasis?

A

Bone metastasis: vertebrae MC site

65
Q

What is the most common cancer metastatic to bone?

A

Breast cancer MC cancer metastatic to bone

66
Q

Describe the connections of the paravertebral venous plexus.

A

Paravertebral venous plexus: connections with vena cava and vertebral bodies

67
Q

What are the first and second most common cancers producing osteoblastic metastases?

A

Prostate cancer MCC osteoblastic metastases, followed by breast cancer

68
Q

What are the lab and radiographic findings of bone metastases?

A

Osteoblastic metastasis: ↑serum ALP; radiodensities in radiographs

69
Q

What are the radiographic findings of osteolytic metastases?

A

Osteolytic metastases: radiolucencies in bone

70
Q

How does a tumor locally activate osteoclasts?

A

PGE2, IL-1 produced by tumor locally activate osteoclasts

71
Q

What are the osteolytic cancers?

A

Osteolytic cancers: lung, kidney, breast

72
Q

What are the clinical findings in osteolytic metastasis?

A

Osteolytic metastasis: hypercalcemia, pathologic fractures

73
Q

How is bone pain in cancer treated?

A

Bone pain: localized radiation

74
Q

What is the most common site for metastasis?

A

Lymph nodes: MC site for metastasis; site of choice for carcinoma

75
Q

What is the second most common cause of death in the U.S.?

A

Cancer: 2nd MCC death in U.S.

76
Q

What is the most common external cause of cancer?

A

Tobacco MC external cause of cancer

77
Q

Name an important risk factor for cancer.

A

Age is an important risk factor for cancer

78
Q

What is the relationship between cancer incidence and age?

A

Cancer incidence increases with age

79
Q

African-Americans have a higher incidence of what two cancers?

A

African-Americans: ↑incidence prostate cancer, multiple myeloma

80
Q

The Japanese have a lower incidence of what two cancers?

A

Japanese: ↓incidence prostate and breast cancer

81
Q

What is the most common cause of disease-related (noninjury) mortality 1-14 years of age?

A

Cancer MCC disease-related (noninjury) mortality 1–14 years of age

82
Q

What are the top three cancers in decreasing order in children?

A

Cancers in children, decreasing order: leukemia, CNS, neuroblastoma

83
Q

How do the locations of cancer in children compare to that in adults?

A

Cancers in children occur in different sites than in adults

84
Q

What are the top three cancers in decreasing order in men?

A

Cancers in men, decreasing order: prostate, lung, colon/rectum

85
Q

What are the top three cancers in decreasing order in women?

A

Cancers in women, decreasing order: breast, lung, colon/rectum

86
Q

What are the top three sites of gynecologic cancers in decreasing order?

A

Sites of gynecologic cancers, decreasing order: endometrium, ovary, cervix

87
Q

What are the top three sites for cancer-related deaths in men in decreasing order?

A

Sites of cancer-related deaths in men, decreasing order: lung, prostate, colon/rectum

88
Q

What are the top three sites for cancer-related deaths in women in decreasing order?

A

Sites of cancer-related deaths in women, decreasing order: lung, breast, colon/rectum

89
Q

What are the top three gynecologic sites for cancer-related deaths in women in decreasing order?

A

Sites of gynecologic cancer–related death, decreasing order: ovary, endometrium, cervix

90
Q

Which cancer is increasing most rapidly worldwide?

A

Malignant melanoma: increasing most rapidly worldwide

91
Q

Describe the epidemiology of cancer in China.

A

China: NP carcinoma (EBV), esophageal SCC (smoking/alcohol)

92
Q

Describe the epidemiology of cancer in Japan.

A

Japan: stomach adenocarcinoma (smoked foods)

93
Q

Describe the epidemiology of cancer in Southeast Asia.

A

Southeast Asia: HCC (HBV postnecrotic cirrhosis, aflatoxins)

94
Q

Describe the epidemiology of cancer in Sub-Saharan Africa.

A

Sub-Saharan Africa: Burkitt lymphoma linked to EBV; KS linked to HHV-8

95
Q

What is the most important prevention modality in cancer?

A

Stop smoking: most important prevention modality

96
Q

How can the risk for colorectal cancer be decreased?

A

↑Dietary fiber, ↓dietary animal saturated fat: ↓risk colorectal cancer

97
Q

How can the risk for oropharyngeal cancer, upper to midesophageal cancer, and HCC be decreased?

A

↓Alcohol intake: ↓risk for alcohol-related cancers

98
Q

How can the risk for estrogen-related endometrial/breast cancer be decreased?

A

Reduce weight: ↓risk estrogen-related endometrial/breast cancer

99
Q

How can the risk for skin cancer be decreased?

A

Sunscreen: ↓risk for BCC, SCC, melanoma

100
Q

What does HBV immunization decrease the risk of?

A

HBV immunization: ↓HCC risk

101
Q

What does HPV immunization decrease the risk of?

A

HPV immunization: ↓risk for cervical/penile SCC

102
Q

What does a cervical Pap detect?

A

Cervical Pap: detects squamous dysplasia → precursor for SCC

103
Q

What is the purpose of a colonoscopy?

A

Colonoscopy detects/removes precancerous polyps

104
Q

What does mammography detect?

A

Mammography detects nonpalpable breast masses

105
Q

Compare the sensitivity and specificity of serum PSA for the diagnosis of prostate cancer.

A

Serum PSA: more sensitive than specific for Dx prostate cancer

106
Q

What does treatment of H. pylori infection decrease the risk of?

A

Rx H. pylori infection: ↓risk gastric lymphoma

107
Q

What does treatment of GERD decrease the risk of?

A

Rx GERD: ↓risk distal adenocarcinoma in esophagus

108
Q

What are the types of gene mutations producing cancer?

A

Point mutations, balanced translocations, insertion viral genome, deletion, amplification, overexpression

109
Q

What are proto-oncogenes involved in?

A

Proto-oncogenes: involved in normal growth/repair

110
Q

What do mutations in proto-oncogenes result in?

A

Mutations in proto-oncogenes: sustained activity of the gene

111
Q

What is the function of tumor suppressor genes? What are the main sites of control in the cell cycle?

A

Suppressor genes: prevent unregulated cell growth; G1 to S phase, nuclear transcription

112
Q

What do mutations in tumor suppressor genes result in?

A

Mutations in suppressor genes → unregulated cell growth

113
Q

What is the function of the BCL2 gene family?

A

BCL2 gene family: antiapoptosis genes; prevent cytochrome c from leaving mt

114
Q

What does the t(14;18) translocation in B cells cause?

A

t(14;18) translocation in B cells: overexpression mutation → B cell follicular lymphoma

115
Q

What is the function of DNA repair genes?

A

Repair genes: correct errors nucleotide pairing; excise pyrimidine dimers

116
Q

What are the enzymes in DNA repair?

A

Enzymes in DNA repair: endonuclease, exonuclease, polymerase, ligase

117
Q

What is the effect of mutations involving DNA repair genes?

A

Mutations DNA repair genes: allow cells with nonlethal damage to proliferate

118
Q

What is the most common carcinogen in the U.S.?

A

Polycyclic hydrocarbons in tobacco smoke MC carcinogen

119
Q

What do direct-acting carcinogens react with? Give an example.

A

Direct-acting carcinogens react with DNA (e.g., alkylating agents)

120
Q

What do indirect-acting carcinogens require? Give an example.

A

Indirect-acting carcinogens require metabolic conversion (e.g., polycyclic hydrocarbons)

121
Q

Describe the sequence of chemical carcinogenesis?

A

Chemical carcinogenesis: initiation → promotion → progression

122
Q

Describe the initiation of chemical carcinogenesis. Give an example.

A

Initiation: irreversible mutation; e.g., ionizing radiation

123
Q

Describe the promotion of chemical carcinogenesis. Give an example.

A

Promotion: proliferation mutated cell; promoters (e.g., estrogen) cannot induce cancer

124
Q

Describe the progression of chemical carcinogenesis.

A

Progression: development of tumor heterogeneity

125
Q

What is the only bacteria that produces cancer?

A

H. pylori only bacteria that produces cancer

126
Q

Which parasite causes SCC in the bladder?

A

S. haematobium: SCC in bladder

127
Q

Which parasites cause cholangiocarcinoma of the bile ducts?

A

Clonorchis sinensis, Opisthorchis viverrini: cholangiocarcinoma bile ducts

128
Q

What are the oncogenic microbial agents in cancer in decreasing order?

A

Oncogenic microbial agents and cancer: viruses > bacteria > parasites

129
Q

What is the most common cancer due to ionizing radiation?

A

Leukemia: MC cancer due to ionizing radiation; AML/CML

130
Q

What are the ionizing radiation-induced cancers in addition to leukemia?

A

Ionizing radiation: papillary cancer thyroid; lung, breast, bone cancers; liver angiosarcoma

131
Q

How does UVB light affect DNA?

A

UVB light produces pyrimidine dimers that distort DNA

132
Q

What is the most common cancer due to excessive UV light exposure? What other cancers may result?

A

BCC: MC cancer due to excessive UV light exposure; others—SCC, melanoma

133
Q

What cancers are associated with physical injury?

A

SCC: 3rd-degree burn scars; orifice of draining sinus

134
Q

What is the most effective host defense against cancer?

A

Cytotoxíc CD8 T cells: most effective host defense

135
Q

How do NK cells kill malignant cells?

A

NK cells kill cell directly (type IV HSR)/indirectly via type II HSR

136
Q

What is more important than grade of cancer?

A

Stage more important than grade of cancer

137
Q

A malignant tumor ≥2 cm has the inherent ability to do what?

A

Malignant tumor ≥2 cm: inherent ability to metastasize

138
Q

Describe staging in order of decreasing prognostic significance.

A

Staging in order of decreasing prognostic significance: M > N > T

139
Q

Name a complication of disseminated cancer.

A

Cachexia is complication of disseminated cancer

140
Q

What is cachexia?

A

Catabolic process including anorexia, muscle wasting, body fat loss

141
Q

What does PIF do?

A

PIF causes degradation of skeletal muscle

142
Q

What are the functions of LIF?

A

LIF ↓body fat; ↑TNF suppresses appetite/initiates apoptosis

143
Q

What is the most common anemia in malignancy?

A

ACD MC anemia

144
Q

Iron deficiency is most often due to what?

A

Iron deficiency: usually colorectal cancer

GI blood loss (e.g., colorectal cancer)

145
Q

Describe the cause of macrocytic anemia in malignancy.

A

Macrocytic anemia: folic acid deficiency; tumor uses folic acid for DNA synthesis

146
Q

What is the cause of cold AIHA in malignancy? Which malignancy is associated with cold AIHA?

A

Cold AIHA: IgM cold agglutinins (CLL)

147
Q

What is myelophthisic anemia?

A

Myelophthisic anemia: marrow replacement by cancer and/or fibrous tissue

148
Q

What are the lab findings in myelophthisic anemia?

A

Immature normal cells in peripheral blood; teardrop cells

149
Q

What adjective describes hemostasis in malignancy?

A

Hemostasis in malignancy: thrombogenic

150
Q

Why is there increased risk for vessel thrombosis in malignancy?

A

Thrombocytosis, ↑coagulation factors, procoagulants from cancer cells

151
Q

What is the cause of DIC in malignancy?

A

DIC: intravascular coagulation due to cancer releasing tissue thromboplastin

152
Q

What is a common cause of death in cancer?

A

Gram-negative sepsis: common cause of death in cancer

153
Q

What is a paraneoplastic syndrome?

A

Paraneoplastic syndrome: distant effects unrelated to metastasis

154
Q

What does a cytokeratin positive stain indicate?

A

Cytokeratin +: epithelial tissue origin

155
Q

What does a vimentin positive stain indicate?

A

Vimentin +: connective tissue origin

156
Q

What does a CD45 positive stain indicate?

A

CD45 +: malignant lymphoma

157
Q

What are tumor markers used for?

A

Markers: Dx cancer, estimate tumor burden, detect recurrences, follow tumor response to therapy

Rapid Review Pathology (14 decks)

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