Dr. A's Pathophysiology 2nd Exam
Quiz yourself by thinking what should be in
each of the black spaces below before clicking
on it to display the answer.
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| What is neoplasia? | New growth (any new growth) that usually refer to solid new growth.
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| What is neoplasm? | mass/tumor
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| What is a benign neoplasm? | A neoplasm that cannot invade
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| What is malignant neoplasm/cancer? | A neoplasm that can invade. Extends into tissues it shouldn't. Crossing over basement membrane, 100% dysplastic
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| What is differentiation in neoplasia? | Degree of resemblance of a tissue to the tissue of origin.
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| What is a well-differentiated neoplasm? | A neoplasm that looks like the tissue of origin.
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| What is a poorly-differentiated neoplasm? | A neoplasm that does not resemble the tissue of origin.
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| What is an undifferentiated/anaplastic neoplasm? | A neoplasm that has no resemblance to any tissue -> tissue won't be able to do what it's supposed to do.
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| Would a patient with a well-differentiated or one with a anaplastic neoplasia be more likely to survive longer? | Well-differentiated are more likely to survive longer.
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| What is cellular pleomorphism and/or tumor giant cells? | Both cellular and nuclear, pleomorphism is more parts of chromosomes or new ones
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| What is hyperchromatism of nuclei? | Dark nuclei b/c they are dividing.
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| What are 7 terms used to define cells in anaplasia? | Cellular pleomorphis/tumor giant cells
Hyperchromatism of nuclei
Prominent nucleolus
Frequency of mitosis
Presence of giant and bizarre appearing nuclei (nuclear pleomorphism)
Disorientation of cells/loss of architecture
Metastasis
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| What is parenchyma? | The proliferating neoplastic cells (by which the tumor is named).
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| Qhat is Supportive stroma? | fibrous connective tissue and blood vessels allowing the neoplasm to persist.
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| If stromal component is minimal the neoplasm will be _____ and ______. | soft and fleshy
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| What is it called if there is an abundance of stroma neoplasm that is dense and hard? | Desmoplasia
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| What 4 types of cells have a normal turnover? | Respiratory epithelium
GI linings
Genito-urinary tract
Mammary gland
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| What are 9 categories of tissue that have normal turnover of cells? | Epithelial linings
Glandular linings
Skin
Ovary and testis
Bone Marrow
Myoblasts
Fetal tissues
Organ hyperplasia
Wound healing
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| A non-glandular benign neoplasm is called what? | Epithelioma or papilloma
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| What is a malignant non-glandular neoplasm called? | Carcinoma
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| What is a glandular benign neoplasm called? | adenoma
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| What is a malignant glandular neoplasm called? | Adenocarcinoma
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| Epithelial neoplasias account for _____ of all neoplasias. | 85%
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| What is carcinoma? | A malignant non-glandular neoplasia of epithelial origin.
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| What is a epithelioma or papilloma? | A benign non-glandular neoplasia of epithelial origin.
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| What is an adenocarcinoma? | A malignant gladular neoplasm of epithelial origin.
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| What is an adenoma? | A benign glandular neoplasm of epithelial origin.
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| What do we call a benign fibrous tissue neoplasia? | Fibroma
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| What do we call a malignant fibrous tissue neoplasia? | Fibrosarcoma
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| What do we call a benign fat neoplasia? | Lipoma
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| What do we call a malignant fat neoplasia? | Liposarcoma
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| What do we call a benign vascular tissue neoplasia? | Angioma
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| What do we call a malignant vascular tissue neoplasia? | Angiosarcoma
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| What to we call a benign smooth muscle neoplasia? | Leiomyoma
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| What do we call a malignant smooth muscle neoplasia? | Leiomyosarcoma
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| What do we call a benign striated muscle neoplasia? | Rhabdomyoma
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| What do we call a malignant striated muscle neoplasia? | Rhabdomyosarcoma
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| What do we call a benign bone neoplasia? | Osteoma
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| What do we call a malignant bone neoplasia? | Osteosarcoma
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| What do we call a benign cartilage neoplasia? | Chondroma
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| What do we call a malignant cartilage neoplasia? | Chondrosarcoma
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| Mesenchymal neoplasias account for ____ of all neoplasias. | 15%
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| What is a fibrosarcoma? | A malignant fibrous tissue neoplasia of mesenchymal origin.
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| What is a fibroma? | A benign fibrous tissue neoplasia of mesenchymal origin.
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| What is a liposarcoma? | A malignant fat neoplasia of mesenchymal origin.
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| What is a lipoma? | A benign fat neoplasia of mesenchymal origin.
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| What is an angiosarcoma? | A malignant vascular tissue neoplasia of mesenchymal origin.
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| What is an angioma? | A benign vascular tissue neoplasia of mesenchymal origin.
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| What is a leiomyosarcoma? | A malignant smooth muscle neoplasia of mesenchymal origin.
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| What is a leiomyoma? | A benign smooth muscle neoplasia of mesenchymal origin.
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| What is a rhabdomyosarcoma? | A malignant striated muscle neoplasia of mesenchymal origin.
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| What is a rhabdomyoma? | A benign striated muscle neoplasia of mesenchymal origin.
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| What is an osteosarcoma? | A malignant bone neoplasia of mesenchymal origin.
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| What is an osteoma? | A benign bone neoplasia of mesenchymal origin.
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| What is a chondrosarcoma? | A malignant cartilage neoplasia of mesenchymal origin.
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| What is a chondroma? | A benign cartilage neoplasia of mesenchymal origin.
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| What do we call a benign neoplasia of lymphoid tissue and lymphocytes? | Infectious mononucleosis and other lymphoproliferative diseases.
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| What do we call a malignant neoplasia of lymphoid tissue and lymphocytes? | Lymphoma (lymphosarcoma)
Lymphocytic leukemia (B and T cell leukemias)
Reticular cell sarcoma
Hodgkin Disease
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| What do we call a benign neoplasia of the thymus? | Thymoma
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| What do we call a malignant neoplasia of the thymus? | Thymoma
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| What do we call a benign neoplasia of granulocytes? | Granulocytosis
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| What do we call a malignant neoplasia of granulocytes? | Myelogenous leukemia (Granulocytic leukemia)
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| What do we call a malignant neoplasia of plasma cells? | Multiple myeloma
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| What do we call a benign neoplasia of erythrocytes? | Polycythemia vera
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| What do we call a malignant neoplasia of erythrocytes? | Erythroleukemia
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| Hematopoietic neoplasias represent around _____ of all cancers in humans. | 0.5%
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| What is a lymphoma (lymphosarcoma) Lymphocytic leukemia (B and T cell leukemias) Reticular cell sarcoma and Hodgkin Disease | A malignant lymphoid tissue and lymphocyte neoplasia.
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| What is an infectious mononucleosis and other lymphoproliferative diseases? | A benign lymphoid tissue and lymphocyte neoplasia.
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| What is a Thymoma? | It can mean both benign and malignant neoplasia of the thymus.
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| What is myelogenous leukemia (granulocytic leukemia)? | A malignant granulocyte neoplasia.
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| What is granulocytosis? | A benign neoplasm of granulocytes.
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| What is multiple myeloma? | A malignant neoplasm of plasma cells.
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| What is erythroleukemia? | A malignant neoplasm of erythrocytes.
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| What is polycythemia vera? | A benign neoplasm of erythrocytes.
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| What do we call a benign neoplasm of brain glial cells? | Astrocytoma, oligodendroglioma
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| What do we call a malignant neoplasm of brain glial cells? | Glioblastoma multiforme
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| What do we call a benign neoplasm of the meninges? | Meningioma
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| What do we call a malignant neoplasm of the meninges? | Meningeal sarcoma
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| What do we call a benign neoplasm of neurons? | Ganglioneuroma
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| What do we call a malignant neoplasm of neurons? | Neuroblastoma
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| What do we call a benign neoplasm of the adrenal medulla? | Pheochromocytoma
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| What do we call a malignant neoplasm of the adrenal medulla? | Pheochromocytoma
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| What do we call a malignant neoplasm of the retina? | Retinoblastoma
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| What is a retinoblastoma? | A malignant retina neoplasm.
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| What is a pheochromocytoma? | It can be a benign or malignant neoplasia of the adrenal medulla; would state benign or malignant
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| What is a neuroblastoma? | A malignant neoplasia of neurons.
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| What is a ganglioneuroma? | A benign neoplasia of neurons.
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| What is a meningeal sarcoma? | A malignant neoplasm of the meninges.
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| What is a meningioma? | A benign neoplasm of the meninges.
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| What is a Glioblastoma multiforme? | A malignant neoplasm of brain glial cells.
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| What is a Astrocytoma, oligodendroglioma. | A benign neoplasm of brain glial cells.
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| The term melanoma is always __________ | malignant.
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| What is seminoma? | Malignant testicular cancer
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| Lymphoma is always __________ | malignant.
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| What is a dermoid cyst/teratoma when it is called mature or immature? | A mixed histogenetic originated neoplasia. Mature is benign, immature is malignant.
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| Leukemia is always _________ | malignant.
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| What are 7 characteristics of benign neoplasms? | Generally encapsulated
Non-invasive
Highly differentiated
Few mitotic figures
Slow growth or no net
Little Anaplasia
Non-metastatic
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| What are 7 characteristics of malignant neoplasms? | Non-encapsulated
Invasive
Poorly differentiated
Mitotic figures common
Can have rapid growth
Relatively anaplastic
Metastatic or capapble of becoming so
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| What is invasion and which neoplasms invade? | The infiltration and destruction of surrounding (local) tissue by a neoplasm.
Malignant neoplasms will invade and destroy surrounding tissue.
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| Define metastasis | The invasive nature of neoplasms which allows them to penetrate into blood vessels, lymphatics and body cavities, providing the opportunity for spread of the neoplasm to a distant anatomical territory.
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| Approximately what percentage of new cancer diagnosed patients with malignant neoplasias present with metastases? | 50%; usually has been around a long time and has fooled the immune system
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| What strongly reduces the possibility of a neoplastic cure? | Metastatic spread
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| What are the 3 pathways of metastatic spread? | Direct seeding
Lymphatic spread
Hematogenous spread
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| What is direct seeding with metastatic spread? | A neoplasm that spreads directly to surrounding tissues.
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| What is lymphatic spread with metastases? | A neoplasm that gets into the lymph system then spreads to another area. i.e. breast cancer -> lymphatic channel to axillary lymph nodes
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| What is hematogenous spread with metastases? | A neoplasm gains access to the blood supply then travels down stream. i.e. colon cancer -> liver since veinous drainage goes to the liver.
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| What is the order of cell change when cells are undergoing neoplastic transformation? | Hyperplasia
Metaplasia
Dysplasia
Tumor Giant Cells
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| What is dysplasia redux? | Disorderly but non-neoplastic proliferation of cells; a loss of uniformity of individual cells and a loss of archigtecture; pleomorphism, hyperchromatism, increased mitoses.
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| Dysplasia has 2 options, what are they? | May progress to malignant neoplasia or may revert to normal tissue.
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| What is the sequence of evolution of neoplasias of epithelial cell origin? | Hyperplasia -> Dysplasia -> Carcinoma in situ (pre-invasive malignancy)-> Malignant neoplasia (can cross basement membrane)
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| What are 5 local effects of clinical manifestations of neoplasias? | Swelling, irritation, blood vessel damage, visceral damage, compromised organ function (explanations pg. 23)
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| What are systemic effects from neoplasias contingent upon? | Hormone secreting a substance. i.e. hormone secreting tumors, glandular of epithelial origin
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| A benign tumor gives what kind of hormone secretion? | Indigenous hormone secretion: hormone is native to the tissue of origin
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| A malignant tumor gives what kind of hormone secretion? | Indigenous or ectopic hormone secretion. Ectopic: hormone is not normally produced by that tissue.
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| What is paraneoplastic syndrome? | Syndromes in which symptoms "mask" the underlying neoplasm. i.e. hypercalcemia could be from a bone neoplasm, metastasis to bone or a PTH-secreting tumor.
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| What are endocrinopathies and some examples? | Tend to be ectopic hormone production but can be any hyper- or hypo- secretion. Cushing's Syndrome (ACTH production by lung carcinoma) or hypercalcemia (parathyroid hormone production by lung carcinoma)
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| What are neuromyopathic (myasthenic syndromes) and some examples? | An autoimmune like process. Lung carcinoma tumor cells elicit antibody formation; antibodies to tumor cells "cross-react" with neuronal endings
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| What are vascular disorders with respect to paraneoplastic syndromes? | Thrombosis (Diffuse blood clotting; DIC; Trousseau syndrome) as a result of increased synthesis of coagulation proteins induced by malignant cells.
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| Neoplasia caused by genetic mutation can only be caused when what occurs? | Mutated genes are not repaired and they control cell growth, division and differentiation will give rise to neoplasia.
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| What are DNA point mutations? | A mismatched base pair that could code for a different amino acid
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| What is chromosomal translocation? | When chromosomes exchange genetic material and hybrid chromosomes result.
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| What is gene amplification? | When promoter sequence expresses a gene multiple times.
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| What can go wrong when DNA mutations occur? (4) | 1. Inherent or induced initial non-random genetic instability
2. Progressive random genetic instability
3. Point mutations and failure to repair DNA
4. Translocations and inversions of chromosomal material
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| If Deletions occur because of DNA mutations what can happen? | Deletion of:
-entire chromosomes
-parts of chromosomes
-specific genes
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| If Additions occur because of DNA mutations what can happen? | Aberrant chromosome replication: Trisomy & Aneuploidy;
Amplifications and repeats
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| What causes genetic mutation? | Environmental agents (mutagens) and Mutations arising during normal cell metabolism
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| Environmental agents (mutagens) are considered ________ and what are some examples? | Exogenous
chemical carcinogens
radiation
dietary carcinogens
tobacco smoke
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| Mutations arising during normal cell metabolism are considered _________ and what can cause it? | endogenous
free radical-induced mutations
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| What are 3 fundamental genetic characteristics of all neoplasms? | 1. the result of non-lethal genetic damage (acquired or inherited)
2. Normal regulatory genes are principal targets of genetic damage
3. Neoplasia is a multi-step process (genotypically as well as phenotypically) = tumor progression
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| What are some normal regulatory genes that are targets of genetic damage? | Proto-oncogenes (growth promoting genes)
Anti-oncogenes (growth inhibiting; aka cancer suppressor genes)
Genes that control apoptosis may be involved
Genes that regulate DNA repair
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| Review pictures and your own drawings | pg 28 - 30
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| What do onco-proteins do? | Do not have important regulatory functions. Do have production in transformed cell does not depend on growth factors or other external signals.
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| What are oncogenes? | Genes which promote neoplastic growth. These genes exist as mutations of naturally occurring proto-oncogenes.
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| What are proto-oncogenes? | Cellular genes that promote normal growth and differentiation.
May become oncogenic by viral or other exogenous influences.
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| What are growth factors as a class of oncogenes? | Polypeptide variants of growth factors which normally stimulate proliferation of cells.
Mutations of genes that encode growth factors render protein products oncogenic either by overexpression or increased binding capacity.
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| What are growth factor receptors as a class of oncogenes? | Transmembrane proteins w/ external ligand binding domain & cytoplasmic tyrosine kinase domain -> transient 2nd messenger activity.
Oncogenic receptors differ: they either overexpress or demonstrate persistent activation of enzyme activity.
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| What are membrane associated signal transduction proteins as a class of oncogenes? | Family of proteins: ras protein is most studied. 10-20% of all human cancers contain ras mutations. ras mutation that contributes to neoplasia is a mutation that maintains ras protein in an activated state.
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| What are nuclear regulatory proteins as a class of oncogenes? | Proteins which are localized in the nucleus and which bind to DNA and activate transcription of proto-onco-genes.
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| What does oncogenes operate via "one-hit" hypothesis mean? | Proto-oncogenes obey via a "one-hit" hypothesis; only need to mutate one allele to mess everything up.
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| What are cancer suppressor genes/tumor suppressor genes? | AKA anti-oncogenes; involved in regulation of cell growth via inhibition; inactivation of anti-oncogenes that leads to neoplasia: involves mutations of both alleles = "two-hit" hypothesis: i.e. recessive genes
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| What are some common tumor suppressor genes? (7) | RB (retinoblastoma)
P53 (Li Fraumeni syndrome)
BRCA 1/BRCA 2
NF
WTx
DCC
APC
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| What is RB? | Retinoblastoma: rare childhood cancer. Fuction of RB genes is critical checkpoint in cell cycle, and inactivating mutations in RB permit unregulated cell proliferation. (pg 158 in book)
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| What is P53 (Li Fraumeni Syndrome)? | Multiple spontaneous tumors. "The guardian of the genome" most important/ubiquitous must commonly mutated gene in all cancers (70%)
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| What is BRCA1/BRCA2? | Breast carcinoma
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| What is NFx | Neurofibromatosis (elephant man) x=subtypes 1,2,...isoforms
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| What is WTx? | Wilm's tumor - Renal carcinomas
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| What is DCC? | Deleted Colon Carcinoma
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| What is APC? | Adenomatous polyposis coli; colon cancer. Exception to "2-hit" hypothesis when 1 knocked out body tends to produce colon polyps
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| There are 2 possible mechanisms by which the 2-hits occur, what are they? | 1. Germline Mutation, 1 allele normal and other mutated (genetic) somatic mutation occurs w/i and both alleles become mutated.
2. Both alleles normal and somatic mutation mutates 1 then later somatic mutation mutates the other.
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| P53 is like a "spell checker" it normally links cell damage with DNA repair, cell-cycle arrest and apoptosis. If there is damage to DNA what does P53 do? | It is phosphorylated by genes that sense the damage and are involved in DNA repair. It assists in DNA repair by causing G1 arrest and inducing DNA repair genes. If it cannot be repaired P53 tells to induce apoptosis.
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| If there is a homozygous loss of P53, what happens? | DNA damage goes unrepaired and mutations become fixed (permanent) in dividing cells. Mutant cells occur and malignant tumors can result.
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| What 2 genes regulate apoptosis? | bcl-2 anti-apoptotic gene
bax pro-apoptotic gene
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| What does bcl-2 do? | Prevents apoptosis, gene overexpression is found in malignant lymphomas
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| What does bax do? | Encourages apoptosis, when gene deleted can lead to malignancy b/c no message to apoptose.
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| What is programmed cell death dictated by? | An interaction/balance of anti- and pro- apoptotic gene products.
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| What is telemorase? | An enzyme which prevents chromosome shortening by adding nucleotides.
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| As normal cells divide the tips of chomosomes ___________, acting as a ___________. | shorten; cell-clock.
i.e. chromosomes shrink each mitosis and skin shows signs of aging
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| What cells lack telemorase and what does this cause? | somatic cells; eventual cell death
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| What are the 4 "steps" of malignant tumor growth? | 1. Malignant change as a result of genetic mutations
2. Proliferation of the malignant cells with further mutations
3. Invasion of neoplastic cells
4. Distant metastases
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| What are 3 factors influence the growth of a tumor? | 1. Kinetics of tumor growth
2. Dependent on the growth fraction = ratio of cell proliferation to cell loss
3. Cell cycle can be similar to normal cell population or more rapid
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| What is psr? | Probability of Self Renewal; rated between 0 and 1.00
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| What psr would a stable/static tissue have? | 0.5 no net loss no net gain
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| What would a psr of 0.51 indicate? | tissue growing
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| What would a psr of 0.49 indicate? | tissue shrinking
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| What psr range would malignant growth/metastasis occur in? | 0.52 - 0.6; similar metabolic rates to other cells but not dying like epithelial cells
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| Tumor _____________ influences tumor growth, why? | Angiogenesis; role in Oxygen and nutrient supply, role in distant spreading of neoplastic cells, role of growth factors VEGF and FGF. Tumor develops own stroma only older tumors learn this behavior
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| How do tumor progression and genetic instability affect tumor growth? | Tumor progression: pre-neoplastic->benign tumor->invasive. Genetic instability: 1 mutation causes further mutations. The 2 together give the evolution of a tumor; takes time to come together.
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| What are the cellular basis of metastasis of carcinomas? | 1. Detachment of tumor cells from each other (loss of cadherin)
2. Attachment of tumor cells to BM/ECM
3. Secretion of proteolytic enzymes which degrade ECM
4. Movement of tumor cells through BM into vessels: locomotion via cytokines
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| What are the 4 steps that must occur for a carcinoma to become metastatic? | 1. Can fly apart
2. Attach to something else; basement membrane
3. Metalloprotease secreted (usually requires Zn)
4. "reverse inflammation" mobilize into blood vessel (pictures pg 39-41)
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| What are the 4 Most common sites for metastatic dissemination of malignant cells? Why? | Liver, Lung, Bone, Brain;
b/c huge blood supply but brain is last b/c must get through BBB and Lung is most common site
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| What is organ tropism? | Neoplastic cells may have a selective site for metastasis that cannot be explained by natural pathways of drainage.
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| What response do tumors usually elicit? | chronic inflammation; correlated with a better prognosis with some cancers
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| Be able to explain the nude mice study with tumor immunity. | pg. 43
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| What is immunosurveillance? | Recognition and destruction of tumor cells by the immune system.
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| What is the role of TSA (tumor-specific antigens) in tumor immunity? | Exhibit unique antigens unique to a specific tumor - immune system recognition try to target cells. Elicits an immune response.
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| What is the role of TAA (tumor-associated antigens)? | Can be used as markers to measure tumor growth. Doesn't appear to produce an antibody. PSA (Prostate Specific Antigen)
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| What are Natural Killer cells? | (or LAK, lymphocyte activated killer cell; IL-1) can lyse tumor cells without recognizing TSA
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| What do cytotoxic T cells do for tumor immunity? | Recognize TSAs and lyse tumor cells (CD8 + cells)
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| There is an increased frequency of cancer in _____________ hosts. | immunodeficient
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| How does immunosurveillance break down when cancer arises in an otherwise healthy individual? | Selective loss of strong TSA's
Carcinogens or tumor products may suppress tumor response
Tumor cells may kill immune cells
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| Lung cancer is 2x greater in ____________ than ______________ | U.S.; Japan
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| Who is more likely to present with a carcinoma? | Older individuals
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| Who is more likely to present with acute leukemia and brain neoplasm? | the young
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| The top 3 cancer probabilities for men and %s? | 1. Prostate 32%
2. Lung and Bronchus 16%
3. Colon and Rectum 12%
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| The top 3 cancer probabilities for women and %s? | 1. Breast 32%
2. Lung and Bronchus 13%
3. Colon and Rectum 13%
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| Which cancer of the most probable for men and women is the most deadly for both sexes? | Lung and Bronchus followed by sex specific areas in each gender
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| What are inherited cancer syndromes? | Well-defined malignancies in which the inheritance of a single mutant gene (which has been identified) greatly increases the risk of developing a neoplasm.
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| What gene is mutated in childhood retinoblastoma? | Rb
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| What gene is nutated in familial adenomatous polyposis coli? | APC
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| What gene is mutated in Li-Fraumeni syndrome? | p53
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| Cancer incidence is _________ in genetic relatives. | increased; may be specific for one type of malignancy or may be a non-specific increased incidence of malignancy; no consistent link to specific gene mutation
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| What are 8 known or suspected carcinogens? | Tobacco smoke
Dietary carcinogens/insufficiencies
Alcohol
Radiation
Chemicals
Therapeutic drugs
Viruses (HPV, EBV, HBV)
Bacteria (H. pylori)
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| What are associated with specific carcinomas? | Retroviruses
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| What can a low risk strain of HPV cause? | Papilloma (warts)
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| What can a high risk strain of HPV cause? | Cervical carcinoma, oral carcinoma
High risk strains contain different DNA sequences when compared to low risk. High risk viral protein products degrade p53 gene product while low risk do not
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| What does EBV infect? | Epithelial cells and B lymphocytes
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| What does EBV produce in healthy individuals? | Mononucleosis
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| What can EBV cause in immunocompromised individuals? | B cell apoptosis is lost: Burkitt's lymphoma (increased expression of bcl-2 = proliferation); Role in Hodgkin's lymphoma
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| Hepatitis B Virus (HBV) is associated with what cancer? | Hepatocellular carcinoma
Hypothesis is multiple mitoses increases spontaneous mutations.
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| What cancers is H. Pylori connected to? | Gastric carcinomas and B-cell lymphomas
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| What are 5 risk factors in pathogenesis of breast/cervical/uterine neoplasias? | Increasing age
Increased length of reproductive life
Decreased number of children
Obesity
Genetics
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| What is the length of survival for prostate cancer? | 12 years whether tx or not
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| What are 5 treatments for prostatic carcinoma? | Watchful waiting
*surgery (Trans Urethral Resection of Prostate)
*Brachytherapy
*External Radiation
Hormone Therapy
*complications=impotence and incontinence
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| What is the gleason grading system? | Prostate only. Histological scores on 2 biopsies b/w 1 and 5. Add both together to get score b/w 2 and 10. Lower the number the better the prognosis.Score based on deviation from normal architecture and relative loss of complete "gland units."
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| What 5 non-neoplastic disorders are associated with malignancy? | Bronchial metaplasia
Endometrial hyperplasia
Liver cirrhosis
Chronic atrophic gastritis
Ulcerative colitis
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| What benign neoplasm has a well defined association with malignancy? | Adenoma of the colon (already affected APC genes)
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| What are the 2 events that allow proliferation to occur? | 1. Initiation: exposure of cells to an appropriate dose of a carcinogenic agent (the initiator) which elicits a permanent DNA mutation
2. Promotion: Upon exposure of initiated cells to a 2nd carcinogen (the promoter), induction of a neoplasm may occur
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| What are 5 common initiators? | 1. Direct alkylating agents
2. Polycyclic aromatic hydrocarbons
3. Aromatic amines and azo dyes
4. Naturally occurring carcinogens; aflatoxin
5. Nitrosamines and amides
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| What is grading of neoplasms? | Based on the degree of differentiation of tumor cells and the number or mitoses within the tumor. A histological method and criteria depends on the tissue. Grade I is well differentiated and Grade IV is poorly differentiated and anaplastic
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| What is staging of neoplasms? | Based on the size of the primary neoplasm, the extent of its spread to regional lymph nodes and the presence or absence of metastases. TNM system
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| The T in neoplasm staging indicates what and is measured how? | Tumor size (0-4)
0 is very small and 4 is relatively large, usually >5cm diameter
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| The N in neoplasm staging indicates what? | Regional lymph node involvement (0-3)
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| What does N0 mean in neoplasm staging? | No nodal involvement; no infiltration to nodal system.
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| What does N1 mean in neoplasm staging? | 1 node or 1 region of nodes infiltrated
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| What does N2 mean in neoplasm staging? | 2 nodal sites affected on 1 side of the diaphragm (upper or lower half)
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| What does N3 mean in neoplasm staging? | Multiple nodal sites affected on both sides of the diaphragm; more clinically advanced
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| The M in neoplasm staging means what and is measured how? | The presence or absence of metastases. 0 (absent) - 1 (present). Typically non-lymphatic tissues
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| The M in staging is important for what 3 specific reasons? | Most diagnostic and prognostic significance
Greatest prediction of long term survival
Survival rates plummet once metastasis occurs
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| What does T0M0N0 mean? | Carcinoma in Situ
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| What are 3 histological/cyological methods used to dx cancer? | Excision or biopsy
Needle aspiration
Cytologic smears
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| What is immunocytochemistry in reference to dx cancer and what is it used with? | Antibody to a specific cell is applied to cells to see how they act. Done with HER2 if the cells light up have HER2 gene mutation
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| What other cancer diagnostics are available? | Molecular identification
Flow cytometry
Tumor markers (PSA)
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| What supports the diagnosis of a neoplasm, monitors progress of treatment and detects recurrence? | Tumor Markers
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| What estrogen receptor is a biochemical indicator of the presence of a tumor? | HER2 = breast carcinoma
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| What is a biochemical indicator of the presence of a liver or testicular tumor? | Alpha-fetoprotein (AFP)
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| What is a biochemical indicator of the presence of a colon, pancreas, or breast carcinoma? | Carcinoembryonic antigen (CEA)
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| What is a biochemical indicator of the presence of a prostate carcinoma? | PSA
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| What is a biochemical indicator of the presence of a Ovarian carcinoma? | CA125
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| Understand the treatment modalities that are currently available. | pg. 64
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| What is leukopenia, what is it due to, it's most common cause, it's association with and symptoms? | Decreased circulating WBCs
Reduced production or accelerated destruction of WBCs
Chemotherapeutics (all cells affeced = aplastic anemia)
Increased infections
Malaise, chill, fever
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| What is Leukocytosis? | Increased circulating number of mature non-neoplastic WBCs. Resembles leukemia
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| What is lymphadenitis? | Inflammation of lymph nodes (acute or chronic); painful and enlarged
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| What is lymphadenopathy? | Enlarged/swollen lymph nodes; non-painful; associated moreso with neoplastic condition
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| What is lymphadenitis almost always see with? | Lymphadenopathy; co-presentation
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| What can occur independent of lymphadenitis? | Lymphadenopathy
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| What are leukemias? | Neoplastic disorders of uncontrolled proliferation of hematopoietic stem cells characterized by replacement of bone marrow with malignant cells. Leukemic cells spill into blood and may infiltrate visceral organs
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| How are leukemias classified? | The basis of cell type involved and based on state of maturity of cell/clinical presentation.
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| If a leukemia is derived from a lymphoid stem cell what is it called? | Lymphocytic leukemia
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| If a leukemia is derived from a myeloid stem cell (granulocytes, monocytes, megakaryocytes) what is it called? | Myelogenous leukemia
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| An acute leukemia means what? | Abrupt, fulminant onset; less differentiated, less mature, more aggressive
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| A chronic leukemia means what? | Slower, indolent progress; more mature
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| What are 4 types of leukemias? | ALL: Acute Lymphocytic Leukemia
AML: Acute Myelogenous Leukemia
CLL: Chronic Lymphocytic Leukemia
CML: Chronic myelogenous Leukemia
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| What are the histological features of acute leukemias? | Immature neoplastic cells due to block in differentiation of stem cell precursor
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| What are the clinical features of acute leukemias? | Abrupt, stormy onset, fulminant clinical course, fatal in untreated pt.s. Symptoms related to depression of normal marrow function: fatigue, fever, bleeding, bone pain, organomegaly, CNS involvement
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| What are the histological features of chronic leukemias? | More well-differentiated, mature leukocytes, predominantly granulocytes
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| What are the clinical presentations seen with chronic leukemias? | Insidious onset, rather slow, indolent clinical course (some can become acute), elevated WBC count, none or vague symptomology = anemia, fatigue and weakness, weight loss, organomegaly
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