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Pathology > Neoplasia > Flashcards

Neoplasia Flashcards

1
Q
  1. Definition of neoplasia?
  2. What is a subclone?
  3. Benign vs malignant?
  4. What is tumor parenchyma?
  5. What is tumor stroma?
A
  1. Process of new growth
  2. Develop from an original clone - mutated cel
  3. Benign - slow growing, well differentiated, and non invasive. Malignant - cancerous
  4. Proliferating neoplastic cells
  5. Supporting connective tissue and blood vessels
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2
Q

CT origin

  1. Benign from: a) fibroblasts b) adipose c) cartilage d) bone
  2. Malignant from: a) fibroblasts b) adipose c) cartilage d) bone
A
  1. a) fibroma b) lipoma c) chondroma d) osteoma
  2. a) fibrosarcoma b) liposarcoma c) chondrosarcoma d) osteogenic sarcoma
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3
Q

Benign Endothelial cells

  1. Blood vessels?
  2. Lymph vessles?
  3. Brain bag?
A
  1. Hemangioma
  2. Lymphangioma
  3. Meningioma
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4
Q

Malignant Endothelial Tissue

  1. Blood vessels?
  2. Lymph vessles?
  3. Synovium?
  4. Mesothelium?
  5. Brain bag?
A
  1. Angiosarcoma
  2. Lymphangiosarcoma
  3. Synovial Sarcoma
  4. Mesothelioma
  5. Invasive meningioma
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5
Q

Benign from muscle:

  1. Smooth?
  2. Striated?
A
  1. Leiomyoma
  2. Rhabdomyoma
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6
Q

Malignant from:

  1. Hematopoietic cells?
  2. Lymphoid cells?
  3. Smooth muscle?
  4. Striated muscle?
A
  1. leukemia
  2. lymphoma
  3. leiomyosarcoma
  4. rhabdomyosarcoma
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7
Q

Benign from:

  1. Stratified squamos cells?
  2. Lining glands or ducts?
  3. Respiratory?
  4. Renal?
  5. Liver
  6. UT transitional epithelium?
  7. Placental?
  8. Melanocytes?
A
  1. Squamos cell papilloma
  2. Adenoma, papilloma, cystadenoma
  3. Bronchial adenoma
  4. Renal tubular adenoma
  5. Liver cell adenoma
  6. Transitional cell papilloma
  7. Hydatidiform mole
  8. nevus
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8
Q

Malignant from:

  1. Stratified squamos cells?
  2. Lining glands or ducts?
  3. Respiratory?
  4. Renal?
  5. Liver?
  6. UT transitional epithelium?
  7. Placental?
  8. Melanocytes?
  9. Testicular germ cells?
A
  1. Squamos cell or epidermoid carcinoma
  2. adenocarcinoma, papillary carcinoma, cystadenocarcinoma
  3. Bronchogenic carcinoma
  4. Renal cell carcinoma
  5. Hepatocellular carcinoma
  6. Transitional cell carcinoma
  7. Choriocarcinoma
  8. Malignant melanoma
  9. Seminoma or embryonal carcinoma
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9
Q
  1. For mesenchyme derived tumors add ____ at end.
  2. Adenoma is used to describe?
  3. What is a polyp?
  4. What is a malignant polyp called?
  5. What is a papilloma?
  6. What is a cystadenoma?
A
  1. -oma
  2. Benign epithelial neoplasm with glandular morphology and also neoplasm derived from glands
  3. Neoplasm of visible projection above a mucosal surface
  4. Polypoid cancer
  5. Epithelial neoplasm w/ finger like projections
  6. Epithelial neoplasm that forms cystic masses
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10
Q

What is this?

A

Papilloma (notice the finger like projections)

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11
Q

What is this?

A

Adenoma - polyp

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12
Q

Nomenclature Basics

  1. Derived from mesenchymal tissue?
  2. Derived from epithelial tissue?
  3. Glandular morphology?
  4. Squamos cell morphology?
  5. What is a mixed tumor?
  6. What is a teratoma?
A
  1. Sarcomas
  2. Carcinomas
  3. Adenocarcinoma
  4. Squamos cell carcinoma
  5. Differentiation of a clone of parenchymal cells into those of another tissue. Eg. pleomorphic adenoma of a salivary gland
  6. Composed of a variety of parenchymal cell types from more than one germ layer
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13
Q

What are 4 phases of the life cycle?

A
  1. Malignant transfromations of the stem cell
  2. Unrestrained growth of the transformed cell
  3. Local invasion
  4. Metastases to neighboring or distant tissues
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14
Q
  1. What is differentiation? What tumors display this?
  2. What is anaplasia? This is hallmark of?
  3. What occurs to the cells in anaplasia?
  4. What occurs to the nuclei in anaplasia?
  5. Anaplastic tumors contain numerous ____ cells and more importantly unusual ___ ____. There is a loss of polarity and they grow in a ____ manner.
  6. Difference in nuclei of 2 tumor type giant cells?
A
  1. Extent to which neoplastic cells resemble normal cells; benign tumors
  2. Lack of differentiation; malignancy
  3. May be larger or much smaller
  4. Become large and hyperchromic
  5. mitotic; mitotic figures; disorganized
  6. Some have a single large hyperchromic nucleus and other have multiple nuclei
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15
Q
  1. What is dysplasia? How is it characterized?
  2. Dysplastic cells are ___ with hyperchromic nuclei and abundant ___ ___.
  3. What is carcinoma in situ?
A
  1. Disordered growth characterized by a loss of cell uniformity and architectural orientation
  2. pleomorphic; mitotic figures
  3. Dysplastic changes involve the entire epithelium but do not cross the basement membrane.
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16
Q
  1. Benign: surface? Growth? Cut surface? Edge?
  2. Malignant: surface? Growth? Edge?
  3. What is the growth fraction?
  4. Most chemos are active only on?
  5. What are cancer stem cells?
  6. Cancer stem cells may develop as a result of a mutation in?
A
  1. Intact; exophytic (out); homogenous; circumscribed
  2. Ulcerated or cut; endophytic; irregular
  3. The number of tumor cells that are actually dividing
  4. Dividing cells
  5. Cells that sustain tumor growth
  6. A normal stem cell
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17
Q

Invasion

  1. Benign tumors are separated from normal tissue by?
  2. Boundaries of malignant tumors?
A
  1. Fibrous capsule
  2. No anatomical boundaries and often penetrate organ walls
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18
Q
  1. What is the unequivocal marker for malignancy?
  2. What are the three routes of dissemination?
  3. What cavity is most commonly seeded?
  4. What type of cancers usually spread through blood?
  5. With hematogenous spread, are veins or arteries more commonly used? Why? What cancers are most common?
A
  1. Metastasis
  2. Seeding body cavities, lymphatic spread, and hematogenous spread
  3. Peritoneal
  4. Sarcomas
  5. Veins because their walls are easier to penetrate; liver and lungs
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19
Q

Nonhereditary conditions associated with the incidence of cancer are?

A

Geography, obesity, alcohol abuse, smoking, and age

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20
Q
  1. Arsenic - use? Increased risk for?
  2. Asbestos - use? Increased risk for?
  3. Benzene - use? Increased risk for?
  4. Beryllium - use? Increased risk for?
  5. Cadmium - uses? Increased risk for?

6 . Chromium - use? Increased risk for?

A
  1. metal smelting and alloys; lung/skin carcinoma and hemangiosarcoma
  2. construction; lung/GI carcinoma and mesothelioma
  3. solvent; leukemia and Hodgkin lymphoma
  4. Aerospace applications; lung carcinoma
  5. Pigments, batteries, and metal alloys; Prostate cancer
  6. Alloys/paints/pigments; lung carcinoma
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21
Q
  1. Ethylene oxide - use? Increased risk for?
  2. Nickel - use? Increased risk for?
  3. Radon - production from? Increased risk for?
  4. Vinyl chloride - use? Increased risk for?
  5. Three major categories of inherited cancer?
A
  1. sterilizing agent/ripening for fruit; leukemia
  2. batteries; nose and lung carcinoma
  3. Decay of minerals containing uranium; lung carcioma
  4. Refrigerants and adhesives; angiosarcoma and hepatocellular carcinoma
  5. autosomal dominant, familial, and autosomal recessive with defective DNA repair
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22
Q
  1. Retinoblastoma - what occurs?
  2. Familial adenomatous polyposis/colon cancer - presentation?
  3. Breast/ovarian councer - gene mutation?
  4. Hereditary nonpolyposis colon cancer - associated with defective?
A
  1. Large masses that may fill the vitreous cavity, necrosis, and calcifications, retinal detachment, and lens displacement forward
  2. Multiple colon adenomas at birth
  3. BRCA1 or BRCA2
  4. Defective DNA repair
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23
Q
  1. Fanconi anemia - characterizations?
  2. Ataxia - telangiectasia - characterization?
  3. Xeroderma pigmentosum - defect in repair of? Characterization
A
  1. Progressive pancytopenia, anemia, congenital abnormalities, increased chromosomal fragility, increased incidence of leukemia
  2. Thymic hypoplasia, cerebellar ataxia, telangiectasias of skin and eyes, and increased incidence of leukemia and lymphoma
  3. UV-induced DNA damage; photosensitivity, increased incidence of basal and squamos cell carcinoma and malignant melanoma
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24
Q
  1. What are some normal regulatory genes that are the targets of mutation?
  2. Fundamental changes in cellular physiology that characterize the malignant phenotype?
A
  1. growth-promoting proto-oncogenes, growth inhibiting tumor suppressor genes, genes that regulat apoptosis or DNA repair
  2. self-sufficiency in growth signals, limitless replicative potential, insentitivity to growth-inhibitory signals, resistance to apoptosis, defective DNA repair, sustained angiogenesis, ability to invade and metastasize
25
Q
  1. In G1: cyclin __/___ complex phosphorylates ___ releasing it from transcription factor ___ allowing it to induce transcriptional activity and allowing the cell to proceed to the S phase.
  2. Progression through S requires cyclin ___/____.
  3. Progression through G2 and M is mediated by?
  4. Progression beyond prophase is mediated by?
  5. What cyclin complex initiates mitosis?
A
  1. D/cdk4,6; RB; E2F
  2. E/cdk2
  3. Cyclin A/cdk2
  4. Cyclin B/cdk1
  5. Cyclin B/cdk1
26
Q
  1. What two tumor suppressors inactivate the cyclin/cdk complexes?
  2. Functions of p53?
  3. What competes with cyclin D for binding to cdk4,6? What does this cause?
  4. What inhibits p53 degradation? How?
A
  1. p27 and p21
  2. Activate transcription of the p21 gene and induce cell cycle arrest and apoptosis in response to DNA damage
  3. p16INK; inhibits RB phosphorylation and causes arrest in G1
  4. p14ARF; by enzyme MDM2
27
Q
  1. What are oncogenes?
  2. What allows malignant cells to be self-sufficient with regards to growth?
A
  1. Promote autonomous growth of cancer cells
  2. Oncogene products
28
Q

Some cancer cells develop ability to synthesize and secrete growth factors:

  1. PDGF is overexpressed in?
  2. Fibroblast growth factors are overexpressed in?
  3. TGFalpha is overexpressed in?
  4. Hetatocyte growth factor is overexpressed in?
A
  1. astrocytomas and osteosarcomas
  2. stomach cancers (and some melanomas, bladder, and breat cancers)
  3. astrocytomas and hepatocellular carcinomas
  4. thyroid cancers
29
Q
  1. EGF receptor is over expressed in?
  2. What is used to treat metastatic Her-2+ breast cancer?
  3. CSF-1 receptor is mutated in?
  4. Neurotrophic factor receptors are mutated in?
  5. PDGF receptors are overexpressed in?
  6. Stem cell factor receptor is mutated in?
A
  1. squamos cell carcinoma of the lung and certain gliomas and breast/ovarian cancers
  2. trastuzumab
  3. myeloid leukemias
  4. neuroendocrine neoplasia and familial medullary thyroid carcinomas
  5. certain gliomas
  6. GI stromal tumors
30
Q
  1. RAS activation is associated with?
  2. When activated, RAS exchanges ___ for ___, recruits the MAP kinase activator ___, activating the MAP kinase pathway which promotes _____.
  3. Why is normal activity of RAS short lived?
  4. What occurs with mutant RAS proteins?
A
  1. Proliferative response to a number of growth factors
  2. GTP; GDP; RAF; mitogenesis
  3. Intrisnic GTPase activity stimulated by binding GTPase-activating proteins
  4. They are not stimulated by GAPs and are thus maintained in constant state of activation
31
Q
  1. Example of self sufficiency through changes to nonreceptor protein kinases?
  2. Self sufficiency though alteration in transcription factors example?
  3. Example of alteration in cell cycle regulators?
A
  1. Reciprocal translocation between chromosomes 9/22 in chronic myeloid leukemia
  2. MYC transcriptional activator is involved in a number of tumors
  3. Abnormalities in expression of cyclin D and E and cdk4 favors neoplastic transformation
32
Q

Defects in tumor suppressor genes cause insensitivity to ___ ___ signals. A model is Retinoblastoma and the ___ gene. Mutations in this gene are also associated with ___ and carcinomas of the ___, ___, and lung. Since this protein is expressed in all cells, it is a good target. In retinoblastoma, ___ ___ of the locus must be mutated. Cancer only develops when the cell becomes _____ for the mutant gene: a process known as the ___ of _____.

A

growth inhibitory; RB; osteosarcoma; breast; colon; both alleles; loss; heterozygosity

33
Q

RB in cell cycle regulation: GF signaling leads to activation of cyclin___/____ complexes that phosphorylate ___, inactivating it and releasing ___ to induce target genes. Note that various growth ___ are associated with ___ RB inactivation.

A

D/cdk4,6; RB; E2F; inhibitors; blocking

34
Q
  1. Mutations in the APC/B-catenin (WNT) pathway are associated with ___ and carcinomas of the ___, ___, and ____.
  2. What is B-catenin?
  3. In the absence of WNT stimulation, most catenin is involved in? Free catenin is bound by? and then?
  4. What occurs when WNT binds to the receptor?
  5. What occurs if APC is mutated?
A
  1. melanomas; stomach; colon; pancreas
  2. transcription factor and mediator of cell adhesion
  3. Intercellular signaling through cadherins; APC; degraded
  4. Stimulates the disocciation of APC-catenin, promoting the migration of catenin to the nucleus where it activates genes associated with proliferation
  5. Catenin is allowed to induce continual proliferation
35
Q
  1. TGFb receptor - pathway normally responsible for? Mutations lead to?
  2. Cadherins - normal function? Loss or malfunctions promotes? Mutations are associated with?
  3. NF-1 gene - neurofibromin normally inhibits? Mutations are associated with?
  4. NF-2 gene - merlin normal function? Mutations result in?
A
  1. Growth inhibition; colon, stomach, and pancretic cancers
  2. Epithelial cell adhesion; malignant phenotype by allowing cells to disaggregate; stomach, esophageal, colon, breast, ovarian, and prostate cancer
36
Q
  1. WNT-1 - normal function? Mutations associated with the development of?
  2. p16INK4 normally blocks? Mutations are associated with?
  3. VHL protein forms complexes that function as? Main substrate? Substrate regulates? Mutations prevent?
A
  1. transcription factor involved with renal and gonadal differentiations; Wilms tumor
  2. CyclinD/cdk4 activity; melanomas and adenocarcinomas
  3. Ubiquitin ligases; HIF; VEGF and PDGF; degradation of HIF-1 and allow uncontrolled growth factor production
37
Q
  1. p53 is normally rapidly degraded by its association with?
  2. Under conditions of stress, what is the function of p53?
  3. What can bind p53 and inactivate it?
  4. p53 links cell damage with?
  5. If damage isnt repaired ___ gene transcription is induced and binds ____ and promotes ____.
A
  1. MDM2
  2. Induce cell cycle arrest and genes associated with DNA repair or apoptosis
  3. HPV E6
  4. DNA repair, cell cycle arrest, and apoptosis
  5. BAX; BCL-2; apoptosis
38
Q
  1. Hereditary nonpolyposis colon cancer: inheritance pattern? Carinoma of? Defect in? Errors accumulate in many genes including?
  2. Xeroderma pigmentosum: inheritance pattern? Risk for developing cancer of the ___ associated with ___ __ causing ___ cross-links that are repaired by ___ ___ repair and individuals with this diesase have defects in this process.
A
  1. autosomal dominant; colon; mismatch repair; proto-oncogenes and tumor suppresor genes
  2. autosomal recessive; skin; UV light; pyrimadine; neuclotide excision
39
Q
  1. Bloom syndrome: inheritance pattern? Defective? This leads to? Patients present with ___ ___ and predisposition to a variety of cancers.
  2. Ataxia-telangiectasia: inheritance pattern? Patients are sensitive to ___ __ are susceptible to ___ malignancies. Defect in a pritein kinase that sense? Presentation?
  3. Fanconi anemia - inheritance pattern? Defect in? Presentation?
A
  1. autosomal recessive; DNA ligase 1; developmental defects
  2. autosomal recessive; ionizing radiation; lymphoid; DNA double strand breaks; loss of Purkinje cells in cerebellum (ataxia_ and defective lymphocyte maturation resulting in ID
  3. autosomal recessive; DNA damage repair; developmental defects, pancytopenia, anemia, and increased risk for leukemias
40
Q
  1. BRCA1/2 are associated with what cancers?
  2. Most common breast cancer?
  3. Replicative senescence eventually occurs from?
  4. Loss of __ function results in intiation of apoptosis.
  5. Characteristics of tumor blood vessels?
A
  1. breast, ovarian, prostate, and pancreatic
  2. Infiltrating ductal carcinoma
  3. shortened telomeres
  4. telomere
  5. leak from over production of VEGF and FGF from tumor and inflammatory cells, and they are not morphologically differentiated
41
Q
  1. Two phases of metastasis?
A
  1. invasion of basement membrane and ecm and dissemination (through blood/lymph) and metastatic tumor growth
42
Q
  1. What is important for normal intercellular adhesion?
  2. In several tumors, _____ expression is down regulated causing intercellular connections to? This is followed by?
A
  1. cadherins
  2. E-cadherin; causing them to loosen and facilitate detatchment; followed by the secretion of collagenases and other enxymes that degrade the BM
43
Q

In circulation tumor cells have a tendency to ____. This is often enhanced by platelets forming ___ ___. Tumor cells protect themselved by reducing expression of ___ and shedding ____ (this helps stop __ cell interactions). The process of arrest and extravasation involves integrins, ___, and other adhesion molecules that the tumor used to cross the BM ____.

A

Aggregate; tumor emboli; MHC1; ICAM1; T; CD44; originally

44
Q

Chronic myeloid leukemia

  1. Chromosomes involved? What major thing comes from each chromosome?
  2. They fuse forming the chimeric gene ___-___.
  3. What is special about the resulting protein kinase?
  4. Therapy?
A
  1. 9 and 22; c-abl proto-oncogene on c9 and bcr on c22
  2. bcr-abl
  3. It has unregulated activity and produces unctonrolled stimulation and uncontrolled proliferation of immature granulocytes
  4. imatinib mesylate
45
Q

Follicular lymphoma

  1. Chromosomes? Gene? Function of gene?
  2. Result?
A
  1. 14 and 18; Bcl-2 on c14; apoptosis inhibitor
  2. Increased transcription of Bcl-2 and a reduction in apoptosis
46
Q

Burkitt Lymphoma

  1. The majority of cases are associated with?
  2. Many involve ___ proto-oncogene on chromosome __ being translocated to chromosome ___ and inserted adjacent to?
  3. Result?
A
  1. EBV
  2. c-myc; 8; 14; Ig heavy chain locus
  3. Regulatory sequences in the Ig locus cause overexpression of myc with a resulting sustained stimulation and proliferation of B-like cells
47
Q

Ewing sarcoma

  1. What is this?
  2. Most cases involve a translocation of a transcription factor from cromosome ___ to an insertion point adjacent to the EWS gene on chromosome ___.
  3. The fusion product codes for?
A
  1. aggressive bone cancer
  2. 11; 22
  3. A transcription factor that induces cell proliferation
48
Q
  1. What is tumor “evolution”
  2. Direct acting carcinogens and metabolic processing?
  3. Indirect-acting are ___ and do require metabolic processing. They are usually activated by?
  4. Example of direct acting carcinogens?
  5. Examples of procarcinogens?
A
  1. Cells are selected that can grow fast and avoid the immune system
  2. Dont require metabolic processing
  3. procarcinogens; activated by the same pathways utilized for their detoxification
  4. Alkylating agents - dimethyl sulfate, cyclophosphamide, and chlorambucil
  5. polycyclic and heterocyclic aromatic hydrocarbons (in smoke), aromatic amines (liver cancer) natural plants (aflatoxins induce liver cancer)
49
Q
  1. What occurs in intiation?
  2. What occurs in promotion?
A
  1. Initiated cell must undergo replication so that the carcinogen-modified change becomes permanent
  2. leads to proliferation of the mutated cell with genetic instability
50
Q
  1. UV radiation induces increased incidence of?
  2. Ionizing radiation includes? Mechanism involves? Most common type of cancer associated?
A
  1. squamos and basal cell carcinomas and malignant melanomas of the skin
  2. x-rays, alpha and beta particles; mutagenesis involves hydroxyl free radical injury to DNA; acute leukemia
51
Q

Human Papilloma Virus

  1. Enveloped? Genome?
  2. Most common lesion is associated with ___ hyperplasia and ____. The normal infection results in accumulation of?
  3. In HPV-induced carcinoma what occurs with the genome?
  4. Most common causes of cervical cancer? Anogenital wards?
  5. Function of E6? E7?
  6. Net effect?
A
  1. Non-enveloped; circular dsDNA
  2. epithelial; dysplasia; hyperplastic tissue
  3. it is incorporated into the host genome
  4. HPV 16/18; HPV 6/11
  5. E6- inhibits p53 induced apoptosis; E7- inhibits p53, p21, and RB induced cell arrest
  6. Cell cycle inhibition is reversed and the cell proliferates
52
Q

EBV

  1. Enveloped? Genome?
  2. Infection of?
  3. Most associated cancers?
A
  1. Enveloped; dsDNA
  2. epithelial and B cells
  3. African Burkitt lymphoma and nasopharyngeal carcinoma
53
Q

Kaposi’s Sarcoma

  1. Associated with what important disease?
  2. Lesions are characterized by?
  3. Chronic/Classic KS occurs in who?
  4. Lymphadenopathic KS occurs where? What are the neoplastic cells?
  5. Immunosuppression-associated KS seen in who?
  6. AIDS-associated KS presents with characteristic?
A
  1. AIDS
  2. spindle shaped cells that have both endothelial and smooth muscle markers
  3. older mediterranean men
  4. Africa; lymphoid cells
  5. Transplant patients
  6. skin lesions
54
Q

Hepatitis

  1. HBV: envelope? Genome?
  2. HDV: genome? envelope?
  3. HCV: genome? envelope?
  4. Cancer associated?
A
  1. enveloped; partial dsDNA
  2. circular ssRNA and needs HBsAG for its own envelope
  3. ssRNA; enveloped
  4. hepatocellular carcinoma
55
Q

HTLV-1

  1. Genome? Envelope?
  2. This causes adult __ ___ with the virus targeting what cells?
  3. It induces malignant proliferation of __ cells resulting in?
  4. Smoldering type presentation?
  5. Chronic type presentation?
  6. acute type presentation?
A
  1. two strands of ssRNA; enveloped
  2. T cell leukemia; CD4 and CD8
  3. T; lymphadenopathy, skin lesions, hepatosplenomegaly, and reccurent infections
  4. normal T cell count w/ abnormal cells and skin lesions
  5. lymphocytosis, skin lesions, and involvement of reticuloendothelial tissue
  6. lymphocytosis, skin lesions, and systemic involvement
56
Q

H. Pylori

  1. Gram?
  2. Infection associated with? Chronic inflammation is thought to promote _____.
  3. Acute inflammation –> ____ infection –> chronic ____ –> ____ metaplasia.
A
  1. negative
  2. chronic gastritis; adenocarcinoma
  3. chronic; inflammation; gastric
57
Q

Tumor Ags

  1. Products of mutated oncogenes may enter class I and be presented to ___ cells or class II and presented to ___ cells.
  2. Over expressed self proteins may be recognized by the immune system as ____
  3. Proteins expressed by oncogenic viruses are associated with a normal immune response to?
A
  1. Tc; Th
  2. foreign
  3. Class I presented viral antigens
58
Q
  1. Direct effects: disease may be complicated by pdtn of ___ or ___ by the neoplastic cells. Also further complicated by?
  2. Indirect manifestations include what two things?
  3. Paraneoplastic syndromes are not directly related but cause endocrinopathies such as?
A
  1. hormones or growth factors; ulcers, bleeding, secondary infection, blood vessel rupture, or infarction
  2. cachexia and fever
  3. Ectopic hormone production, cushings (excess cortisol), and inappropriate secretion of ADH
59
Q
A

Pathology (11 decks)

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