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Principles Of Disease > disorders of cell growth (pathology) > Flashcards

disorders of cell growth (pathology) Flashcards

1
Q

Describe the classification of tumors based on tissue of origin.

A

Epithelial tumors (carcinomas) arise from epithelial tissues, while connective tissue tumors (sarcomas) originate from connective tissues like bone, muscle, or cartilage. Hematopoietic and lymphoid tumors arise from blood-forming tissues and the lymphatic system.

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2
Q

What are the two main categories of behavior for tumors?

A

The two main categories of behavior for tumors are benign tumors, which are typically localized and non-invasive, and malignant tumors (cancers), which have the potential to invade surrounding tissues and metastasize to distant sites.

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3
Q

Define differentiation in the context of tumor histological features.

A

Differentiation refers to how closely tumor cells resemble normal tissue cells. Well-differentiated tumors closely resemble normal cells, while poorly differentiated tumors have less resemblance.

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4
Q

How do biomarkers aid in subclassifying tumors and guiding targeted therapies?

A

Biomarkers, which are specific molecular and genetic markers, help identify different subtypes of tumors and guide targeted therapies based on the unique characteristics of the tumor.

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5
Q

Describe the difference between staging and grading of tumors.

A

Staging describes the extent of spread and involvement of surrounding tissues, while grading assesses the degree of abnormality and aggressiveness of tumor cells.

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6
Q

Describe the growth pattern of benign tumors.

A

Benign tumors typically grow in a well-defined, localized manner without invading surrounding tissues.

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7
Q

What does it mean for a benign tumor to be encapsulated?

A

Benign tumors are often encapsulated, meaning they are surrounded by a fibrous capsule that separates them from neighboring tissues.

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8
Q

How do cells in benign tumors differ from normal cells?

A

Cells in benign tumors closely resemble normal cells and are well-differentiated.

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9
Q

Describe the rate of growth of benign tumors.

A

Benign tumors generally grow slowly and tend to have a more predictable rate of growth.

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10
Q

What is the metastatic potential of benign tumors?

A

Benign tumors do not invade nearby tissues or metastasize to distant sites. They remain confined to their site of origin.

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11
Q

What is the mitotic activity like in benign tumors?

A

Benign tumors usually have a lower rate of cell division (mitosis) compared to malignant tumors.

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12
Q

What are the local effects of benign tumors?

A

Benign tumors may cause local effects by compressing nearby structures, but they do not spread to other parts of the body.

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13
Q

Describe the growth pattern of malignant tumors.

A

Malignant tumors invade surrounding tissues and have the potential to infiltrate blood vessels or lymphatics, facilitating metastasis.

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14
Q

Describe encapsulation in the context of malignant tumors.

A

Encapsulation refers to the presence of a well-defined capsule around tumors. Malignant tumors lack this capsule and can infiltrate neighboring tissues.

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15
Q

What is cellular differentiation and how does it relate to malignant tumors?

A

Cellular differentiation refers to how closely tumor cells resemble normal cells. Malignant tumors can range from well-differentiated (resembling normal cells) to poorly differentiated or undifferentiated.

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16
Q

Explain the rate of growth in malignant tumors.

A

Malignant tumors may exhibit variable rates of growth. Some can be highly aggressive with rapid progression.

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17
Q

Describe the mitotic activity in malignant tumors.

A

Malignant tumors often display increased mitotic activity, reflecting their rapid cell division.

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18
Q

What are the local effects and systemic symptoms associated with malignant tumors?

A

Malignant tumors can cause local effects such as tissue destruction and may induce systemic symptoms like weight loss and fatigue.

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19
Q

What is the clinical impact of malignant tumors?

A

Malignant tumors have the potential to be life-threatening if not treated promptly. Treatment may involve surgery, chemotherapy, radiation, or a combination.

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20
Q

Describe uncontrolled proliferation in cancer cells.

A

Uncontrolled proliferation refers to the excessive and abnormal cell division observed in cancer cells, which is a result of the loss of cell cycle control.

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21
Q

What is the significance of autonomous growth signals in cancer cells?

A

Autonomous growth signals in cancer cells refer to their ability to grow and divide without external signals. This insensitivity to growth inhibition signals allows cancer cells to disregard normal growth-regulating signals.

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22
Q

How do cancer cells evade apoptosis?

A

Cancer cells can evade apoptosis, or programmed cell death, which is a natural process that eliminates damaged or abnormal cells. This ability to resist apoptosis allows cancer cells to survive and proliferate despite genetic damage or abnormalities.

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23
Q

Define angiogenesis induction in cancer cells.

A

Angiogenesis induction in cancer cells refers to their ability to stimulate the formation of new blood vessels. This process ensures a blood supply to the cancer cells, facilitating their continued growth and survival.

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24
Q

Describe telomere maintenance in cancer cells.

A

Telomere maintenance in cancer cells refers to their ability to maintain the protective ends of chromosomes called telomeres. This allows cancer cells to avoid the normal process of cellular aging and achieve limitless replicative potential.

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25
Q

What is metastasis in cancer?

A

Metastasis is the ability of cancer cells to spread to distant sites through the bloodstream or lymphatic system, forming secondary tumors in distant organs.

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26
Q

Describe the process of local invasion in cancer.

A

Cancer cells invade surrounding tissues at the primary tumor site by breaking through normal tissue boundaries.

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27
Q

Cancer cells invade surrounding tissues at the primary tumor site by breaking through normal tissue boundaries.

A

Intravasation is the process in which cancer cells invade blood vessels or lymphatic vessels.

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28
Q

What happens during the arrest at a secondary site in cancer?

A

Cancer cells must exit the circulation or lymphatic vessels and adhere to the endothelium at a secondary site.

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29
Q

Describe the role of Matrix Metalloproteinases (MMPs) in cancer.

A

MMPs help cancer cells degrade the extracellular matrix, facilitating invasion and intravasation.

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30
Q

What is the function of angiogenesis in cancer?

A

Cancer cells stimulate the formation of new blood vessels, promoting the establishment of a blood supply for growing metastases.

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31
Q

Define immune evasion in the context of cancer.

A

Cancer cells may evade the immune system at both the primary and secondary sites, allowing them to survive and proliferate.

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32
Q

How does Epithelial-Mesenchymal Transition (EMT) contribute to cancer metastasis?

A

EMT is a process in which cancer cells acquire characteristics that enhance their ability to invade and metastasize.

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33
Q

What is the significance of chemotaxis in cancer?

A

Cancer cells are attracted to specific chemical signals, guiding their migration towards secondary sites.

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34
Q

Describe tissue destruction caused by cancer cells.

A

Cancer cells can invade and destroy nearby normal tissues as they grow, leading to the loss of functional tissue.

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35
Q

What are the effects of tumors exerting physical pressure on surrounding structures?

A

Tumors can cause compression, leading to pain, altered organ function, or obstruction of normal pathways.

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36
Q

How does cancer-related pain occur?

A

Cancer-related pain can from tissue invasion, compression of nerves, or the release of substances that stimulate pain receptors.

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37
Q

Define obstruction caused by tumors.

A

Tumors in hollow organs or passageways can obstruct the normal flow of fluids, such as urine or blood, leading to issues like urinary obstruction or vascular compromise.

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38
Q

Describe how tumors can lead to ulceration.

A

Some tumors can ulcerate the overlying skin or mucous membranes, leading to open sores that may be prone to infection.

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39
Q

How can tumors lead to functional impairment?

A

Depending on the location, tumors can impair the normal function of organs and tissues. For example, a lung tumor may affect breathing, while a brain tumor can impact neurological function.

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40
Q

What is the risk associated with tumors that invade bones?

A

Tumors that invade bones can weaken them, increasing the risk of fractures.

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41
Q

What are the potential effects of tumors compressing or infiltrating nerves?

A

Tumors can compress or infiltrate nerves, leading to neurological symptoms and pain.

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42
Q

Describe weight loss (cachexia) in cancer.

A

Unintentional weight loss accompanied by muscle wasting and weakness in cancer patients.

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43
Q

What is cancer-related fatigue?

A

A pervasive and persistent feeling of tiredness that can significantly impact a person’s quality of life.

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44
Q

How can cancer induce fever?

A

Cancer can induce fever either as a direct effect of the tumor or due to inflammation and immune responses.

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45
Q

Define anemia in the context of cancer.

A

A decrease in red blood cell count resulting in fatigue, weakness, and shortness of breath in cancer patients.

46
Q

What is immune system suppression in the context of cancer?

A

Cancer and its treatments can suppress the immune system, making individuals more susceptible to infections.

47
Q

How can cancer affect the endocrine system?

A

Some cancers can disrupt the normal functioning of the endocrine system, leading to hormonal imbalances.

48
Q

Describe cancer-related cognitive impairment.

A

Cancer-related cognitive impairment, also known as ‘chemo brain,’ can cause difficulties in concentration, memory, and attention.

49
Q

What are some potential mental health issues that can arise from coping with a cancer diagnosis and treatment?

A

Coping with a cancer diagnosis and treatment can contribute to mental health issues such as depression and anxiety.

50
Q

Define thrombosis and hypercoagulability in relation to cancer.

A

Thrombosis and hypercoagulability refer to the increased risk of blood clot formation in cancer patients, which can lead to conditions like deep vein thrombosis (DVT) and pulmonary embolism.

51
Q

Describe dysplasia.

A

Dysplasia refers to the abnormal growth or development of cells within a tissue. It is characterized by changes in the size, shape, and organization of cells.

52
Q

What is the risk associated with severe dysplasia?

A

Severe dysplasia indicates a higher risk of progressing to cancer if left untreated.

53
Q

Define intraepithelial neoplasia (IEN).

A

Intraepithelial neoplasia refers to the abnormal growth of cells within the epithelial layer of an organ or surface without invasion into the underlying tissue.

54
Q

Describe the grading system for intraepithelial neoplasia.

A

Intraepithelial neoplasia is graded based on the degree of cellular abnormality, similar to dysplasia. It can be classified as low-grade or high-grade, indicating the level of risk for progression to cancer.

55
Q

What is the difference between CIN 1, CIN 2, and CIN 3?

A

CIN 1 refers to mild dysplasia, CIN 2 refers to moderate dysplasia, and CIN 3 refers to severe dysplasia or carcinoma in situ.

56
Q

Define dysplasia and intraepithelial neoplasia.

A

Dysplasia is a broader term that describes abnormal cellular changes within epithelial tissues. Intraepithelial neoplasia emphasizes the potential for progression to cancer.

57
Q

Describe the process that occurs during the G1 phase of interphase.

A

Cell growth and normal metabolic processes occur.

58
Q

What is the function of cyclins in the cell cycle?

A

Cyclins are regulatory proteins that control the progression of the cell cycle.

59
Q

Name two key genes involved in DNA replication during the S phase of interphase.

A

DNA polymerase, cyclin A, CDK2.

60
Q

How do tumor suppressor genes function in the cell cycle?

A

Tumor suppressor genes monitor and repair DNA damage, or initiate apoptosis if damage is irreparable.

61
Q

Describe the function of checkpoint genes.

A

Checkpoint genes ensure proper progression through the cell cycle by assessing DNA integrity.

62
Q

Define the role of Retinoblastoma Protein (Rb) in the cell cycle.

A

Rb regulates the G1 to S phase transition by inhibiting CDK4 and CDK6 when unphosphorylated.

63
Q

What is the function of the G1 checkpoint (Restriction Point)?

A

The G1 checkpoint ensures the cell is ready to enter the S phase.

64
Q

How does the G2/M checkpoint contribute to cell cycle regulation?

A

The G2/M checkpoint ensures DNA replication is complete and the cell is ready to enter mitosis.

65
Q

Describe the function of the spindle checkpoint.

A

The spindle checkpoint ensures proper chromosome alignment and attachment to the spindle fibers before cell division.

66
Q

Define oncogenes.

A

Oncogenes are genes that have the potential to cause cancer.

67
Q

How do mutations in oncogenes contribute to uncontrolled cell growth?

A

Mutations in oncogenes can lead to the production of a hyperactive or overexpressed protein that promotes uncontrolled cell growth.

68
Q

What are growth factor receptors and how can their mutation contribute to cancer development?

A

Growth factor receptors, when mutated, can lead to continuous signaling for cell growth, contributing to cancer development.

69
Q

Describe the role of transcription factors in cancer and give examples of oncogenes involved in controlling gene expression.

A

Transcription factors are oncogenes that control gene expression. Mutations in oncogenes like MYC and MYB can contribute to cancer.

70
Q

What are proto-oncogenes and how do they become oncogenes?

A

Proto-oncogenes are genes that have important roles in normal cellular function. They become oncogenes when they acquire mutations that confer a growth advantage to the cell.

71
Q

What are the contributions of oncogenes to cancer?

A

Oncogenes contribute to cancer by promoting cell proliferation, inhibiting apoptosis, and facilitating the survival and growth of cancer cells.

72
Q

Describe the role of tumor suppressor genes in regulating cell division and preventing the formation of tumors.

A

Tumor suppressor genes regulate cell division and prevent the formation of tumors by inhibiting cell proliferation and promoting proper progression through the cell cycle phases.

73
Q

How do tumor suppressor genes contribute to maintaining the integrity of the cell’s genetic material?

A

Tumor suppressor genes are involved in DNA repair mechanisms, ensuring the integrity of the cell’s genetic material.

74
Q

Define apoptosis and explain the role of tumor suppressor genes in this process.

A

Apoptosis is programmed cell death. Tumor suppressor genes play a role in apoptosis by helping eliminate cells with damaged DNA that could potentially become cancerous.

75
Q

Describe the concept of a tumor suppressor gene.

A

Tumor suppressor genes are genes that help regulate cell growth and division, and their loss or mutation can contribute to the development of cancer.

76
Q

What is the role of p53 in the cell?

A

p53 is a crucial tumor suppressor gene that monitors DNA damage and initiates repair processes or apoptosis if damage is severe.

77
Q

Define germline mutation.

A

A germline mutation refers to a genetic mutation that is present in the germ cells (sperm or egg) and can be passed on to offspring.

78
Q

How do mutations in BRCA1 and BRCA2 genes increase the risk of cancer?

A

Mutations in BRCA1 and BRCA2 genes are associated with an increased risk of breast and ovarian cancers as these genes are involved in DNA repair.

79
Q

Describe the function of PTEN gene.

A

PTEN gene regulates cell growth and division, and mutations in this gene are associated with various cancers, including breast, prostate, and brain cancers.

80
Q

What is the significance of both copies of a tumor suppressor gene needing to be mutated or inactivated for the protective function to be lost?

A

Both copies of a tumor suppressor gene need to be mutated or inactivated for the protective function to be lost, ensuring that the loss of function is a rare event and reducing the risk of cancer development.

81
Q

Describe how chemical exposure can increase the risk of cancer.

A

Chemical exposure to substances like tobacco smoke, industrial chemicals, and environmental pollutants can increase the risk of cancer.

82
Q

Define ionizing radiation and explain how it can contribute to the development of cancer.

A

Ionizing radiation, such as X-rays or environmental radiation, can damage DNA and contribute to the development of cancer.

83
Q

How are certain infections linked to cancer development?

A

Certain infections, such as certain strains of human papillomavirus (HPV) and Helicobacter pylori infection, are linked to the development of cervical cancer and stomach cancer, respectively.

84
Q

Describe how genetic mutations can increase susceptibility to cancer.

A

Genetic mutations, whether inherited or spontaneous, can increase an individual’s susceptibility to cancer by altering specific genes that regulate cell growth and division.

85
Q

Do epigenetic changes involve alterations in the DNA sequence?

A

No, epigenetic changes involve alterations in gene expression without changes in the underlying DNA sequence.

86
Q

Describe how a family history of cancer can indicate a hereditary predisposition.

A

A family history of certain cancers can indicate a hereditary predisposition, suggesting the presence of genetic mutations that increase the risk of developing cancer.

87
Q

Describe the multistep nature of carcinogenesis.

A

The multistep nature of carcinogenesis refers to the gradual process by which normal cells transform into cancer cells through the accumulation of genetic and epigenetic alterations over time.

88
Q

What is the initiation stage in carcinogenesis?

A

The initiation stage is the first step in carcinogenesis where exposure to carcinogens or genetic mutations leads to the initial transformation of a normal cell into a precancerous cell.

89
Q

Define promotion in the context of carcinogenesis.

A

Promotion in carcinogenesis refers to the stage following initiation, where the initiated cells undergo expansion and further development.

90
Q

Describe the progression phase of cancer.

A

During progression, additional genetic and epigenetic changes occur, promoting the evolution of precancerous cells into fully malignant cancer cells.

91
Q

Define heterogeneity in the context of cancer.

A

Heterogeneity refers to the genetic and phenotypic diversity observed within a tumor, where different subpopulations of cells may harbor distinct genetic alterations.

92
Q

Define metastasis.

A

Metastasis is the ability of cancer cells to invade surrounding tissues and spread to distant organs, representing a late stage in the multistep process of carcinogenesis.

93
Q

What can happen if the HER2 gene is amplified or overexpressed?

A

Amplification or overexpression of the HER2 gene can lead to uncontrolled cell proliferation.

94
Q

Which cancer is often associated with HER2 overexpression?

A

HER2 overexpression is often associated with breast cancer.

95
Q

Which cancers frequently have mutations in the BRAF gene?

A

Mutations in the BRAF gene are frequently found in melanoma and colorectal cancer.

96
Q

What is the common mutation in the BRAF gene in melanoma?

A

The V600E mutation is common in the BRAF gene in melanoma.

97
Q

Describe the role of the RB gene.

A

The RB gene codes for the retinoblastoma protein, which regulates the cell cycle by inhibiting cell division.

98
Q

Which cancers are associated with RB mutations?

A

RB mutations are found in retinoblastoma, osteosarcoma, and small-cell lung cancer.

99
Q

Describe the role of mismatch repair proteins.

A

Mismatch repair proteins are involved in correcting errors that occur during DNA replication.

100
Q

What is the consequence of deficiencies in mismatch repair?

A

Deficiencies in mismatch repair can lead to the accumulation of genetic mutations.

101
Q

Define p53.

A

p53 is a tumor suppressor gene that regulates the cell cycle, DNA repair, and apoptosis.

102
Q

Which cancers are commonly associated with mismatch repair deficiencies?

A

Mismatch repair deficiencies are commonly seen in hereditary non-polyposis colorectal cancer (HNPCC), endometrial, and ovarian cancers.

103
Q

How do TP53 mutations contribute to cancer development?

A

TP53 mutations can confer a survival advantage to cancer cells by evading apoptosis and promoting genomic instability.

104
Q

Describe the link between smoking and cancer.

A

Tobacco smoke contains carcinogens and smoking is a major risk factor for several types of cancer, including lung, mouth, throat, esophagus, pancreas, bladder, kidney, and cervix.

105
Q

What is the mechanism by which smoking contributes to cancer development?

A

The carcinogens in tobacco smoke can damage DNA in cells, leading to genetic mutations. Chronic exposure to these mutagenic substances contributes to the transformation of normal cells into cancer cells. Smoking also causes inflammation and impairs DNA repair.

106
Q

Describe the link between HPV and cancer.

A

Certain strains of HPV are strongly linked to the development of cervical and other cancers. HPV is a sexually transmitted infection, and persistent infection with high-risk HPV types can lead to the transformation of normal cells into cancerous cells.

107
Q

How does HPV infect the body?

A

HPV primarily infects epithelial cells, primarily in the genital and oropharyngeal areas.

108
Q

What are the types of cancer associated with smoking?

A

Smoking is associated with lung, mouth, throat, esophagus, pancreas, bladder, kidney, and cervix cancers.

109
Q

Describe the mechanism by which high-risk HPV types can lead to cancer.

A

High-risk HPV types can integrate their DNA into the host cell’s genome, disrupting normal cellular control mechanisms. This can lead to uncontrolled cell growth and the development of precancerous lesions that may progress to cancer.

110
Q

What are some cancers associated with excessive and chronic alcohol consumption?

A

Cancers associated with alcohol consumption include those of the oral cavity, pharynx, larynx, esophagus, liver, colorectum, and breast.

111
Q

How does alcohol contribute to cancer development?

A

Alcohol can be metabolized in the body to acetaldehyde, a toxic and carcinogenic substance. Acetaldehyde can directly damage DNA, leading to genetic mutations. Chronic alcohol use can also contribute to inflammation, impair immune function, and interfere with the absorption of essential nutrients, all of which can contribute to cancer development.

Principles Of Disease (11 decks)

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