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42 Cards in this Set
- Front
- Back
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aging brain
thyroid size after pituitary resection what category of cell adaptation? |
atrophy
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protective mechanism that may lead to loss of function
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metaplasia
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myocardial cells in high BP
what category of cell adaptation? |
hypertrophy
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callus
what category of cell adaptation? |
hyperplasia
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sex organs at puberty
what category of cell adaptation? |
hypertrophy
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hormonal stimulation of the endometrium
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hyperplasia
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increase of prostate gland
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hyperplasia
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distinguish aplasia, agenesis, hypoplasia
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Agenesis (complete absence)
aplasia(absent with only rudimentary) hypoplasia- reduced in size, incomplete developement |
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name exceptions to "OMA" that are actually malignant
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melanoma, lymphoma, mesothelioma
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elevated mucosal projection
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polyp
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benign with fingerlike projection
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papilloma
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tumor with mesenchymal origin vs. epithelial origin ...their names
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sarcoma vs. carcinoma
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lack of differentiation
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anaplasia
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extent that tumor resemble the normal cell
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differentiation
(more differentiated, more normally functioning) note: not all well differentiated are benign. |
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true of false
basemembrane is intact in carcinoma in situ |
true.
carcinoma in situ is sever dysplasia...not metasized yet. |
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frequent sites of hematogenous spread
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liver and lung
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four possible cavities involved in seeding
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peritoneum, pleural, pericardium, subarachnoid
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gene types
RAS, ABL |
protoncogenes
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p53, APC, BRCA, RB, WT-1
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tumor suppressor
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BCL-2
what kind? results in what disease |
apoptosis regulating gene, result in lymphoma
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2 sources of angiogenic factors
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tumor cells
inflammatory cells infiltrating tumor |
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this part of tumor determines the growth and progression
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stroma ( cos it supplies blood and nutrient)
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factors involved in invastion of ECM
in detachment, degradation of ECM, attachment, movement |
detachment: decrease cadherin
degredation: collagenase, cathepsin B attachment: laminin receptors, integrin, MMP2/9 establishing new site moving: autocrine motility factors |
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tumor forms this by agregating with platelet and wbc
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emboli
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receptors for homing of breast cancer
ligands that bind there, likely site? treatment option based on this? |
receptor : CXCR 4/7
ligand: CCL12, CCL21 (likely in site for metastasizing) treatment: block the receptor |
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anti tumor mechanisms ( cells involved etc)
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cytotoxic T lymphocytes (CTL)
NK cells Macrophaged (secrete TNF/Free radicals) Humoral destruction by complement |
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used to determine stage of cancer
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TNM
(tumor size - primary lesion, node spread, metastases) |
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which ones more important
grade of stage |
stage (spreading) not grade ( differentiation)
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state tumors that may cause these symptoms
torsion bleeding bowel obstruction destruction of remaining gland press on facial nerve blindness valvular stenosis hemoptysis |
torsion: ovarian
bleeding: leiomyoma, GI, UG, bowel obstruction: gut destruction of remaining gland: pituitary tumor press on facial nerve: parotid gland blindness: choroidal melanoma valvular stenosis: atrial myxoma hemoptysis: lung |
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more on matching with cancer
hypoglycemia+ death 2ndary cushing syndrome increased hormone production |
hypoglycemia+ death: Bcell pancrease adenoma
2ndary cushing syndrome: adrenal cortex increased hormone production : carcinoid tumour |
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unexplained symptom due to tumor spreading to elsewhere in the body ( to different system)
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paraneoplastic syndrome
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which one is paraneoplastic syndrome?
insulin increase in lung vs. in islet cell |
in lung ( because insulin is not normally synthesized in lung)
key phrase for paraneoplastic syndrome- "not original function of the system" |
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form filled out for lab Dx
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properly filled requisition form
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most tissues are fixed in
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10% formalin
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HTLV
type of gene, cancers associated |
retrovirus,
T- cell leukemia/lymphoma |
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most tumors are monoclonal. exceptions
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leukemia- polyclonal
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H. Pylori infectino can lead to
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maltoma ( B cell lymphoma in MALT)
gastritis, gastric cancer |
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t(8:14)
t(9:22) - exmplain path for this one lead to |
t(8:14)- burkitt lymphoma
t(9:22)- CML ( tranlocation--> activated BCR-ABL, protoconcogene--> increase TYROSINE KINASE --> cml) |
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what kind of mutation occur in RAS
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poiny mutation
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gene amplification of cmyc leads to
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neuroblastoma
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NF1, WT1 lead to
what kind of genese are these |
NF1- neurofibromatosis
WT1- wilm's tumor tumor supressor genes |
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BCL-2
what kind of gene? mutation here lead to what tumor? |
apoptosis regulating gene, lead to B- cell lymphomas, chronic lymphocytic leukemia
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