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patho ch 7 altered
| Question | Answer |
|---|---|
| cancer | diseases with uncontrolled proliferation of abnormal cells and spread |
| checkpoint of cell cycle | G1/S and G2/M |
| G1/S | growth phase 1/synthesis (DNA synthesis) |
| G2/M | growth phase 2/mitosis |
| mitosis | nonsex cell |
| meiosis | sex cell (egg/sperm) |
| why is cancer bad for normal cells | crowds out normal cells and competes for nutrients |
| cell differentiation | specialization of cells for specific functions |
| anaplasia | loss of differentiation (resembling primitive form) leads to organ system failure |
| highly anaplastic tumors characteristic | more aggressive and less responsive to normal growth controls |
| stem cells | self renewal capacity and ability to differentiate |
| cancer stem cells | drive tumor initiation and long term growth |
| impact of cancer on stem cells | cancer disrupts balance of stem cells and mature cells |
| how does cancer occur | gene malfunction (alteration of reproductive/growth/differentiation/apoptosis) altered proliferation or altered differentiation |
| neoplasms | irreversible deviant cell clusters, highly invasive and destructive uncontrolled and irregulated |
| where can neoplastic cells originate from | proliferating parenchymal tissue/organ stromal cells (supportive structures) |
| stromal cells | cells that provide structure |
| carcinogenesis | origin and development of cancer due to gene mutations/gene variants/epigenetics |
| 2 major gene mutations | inherited mutations (germ-line) acquired mutations (somatic) |
| acquired mutations | aka somatic mutations, acquired after birth 95% of cases |
| inherited mutations | aka germ line mutation, present in egg/sperm 5% of cases and can be passed to offspring |
| proto-oncogenes | normal growth/survival gene can turn into oncogenes |
| how do proto-oncogenes turn into oncogenes | 1. point mutation 2. chromosomal translocation 3. gene amplifications |
| oncogenes | one activating event in single allele often sufficient (dominant effect) |
| examples of oncogenes | RAS point mutation, MYC overexpression, HER2 amplification |
| tumor suppression genes | inhibit cell division/promotion of apoptosis loss of checkpoints in mutation |
| how are tumor suppressor genes inactivated | biallelic loss (Knudson "two-hit" hypothesis) via mutations, deletions, epigenetic silencing |
| examples of tumor suppressor gene | TP53, Rb gene, BCL-2 (therapies target these mechanisms) |
| DNA repair genes (aka, what it does) | aka mutator/caretaker gene maintain genomic integrity by fixing damaged DNA and maintaining genomic stability |
| how do DNA repair genes maintain genetic integrity | mismatch repair, homologous recombination |
| how are DNA repair genes inactivated | biallelic inactivation or epigenetic silencing accumulation of gene errors |
| polymorphism | gene variants |
| what do gene variants do | influence cancer risk by altering enzyme/hormone function |
| how do epigenetic changes affect proliferation/differentiation | change gene expression does not alter DNA sequence |
| how can gene variants be influenced | DNA methylation, histone modification, RNA interference |
| histones | proteins that help package DNA into chromosomes |
| carcinogens | stuff that can initiate/promote cancer development |
| direct vs indirect carcinogens | direct DNA damage vs chronic inflammation/immunosuppression |
| examples of direct carcinogens | radiation, inhalation (tobacco), chemicals |
| examples of indirect carcinogens | smoked foods, infectious microbes |
| how do hormones function in cancer | some cancers are hormone dependent (ie breast/prostate/thyroid) acts as promoters |
| how are hormone-dependent cancers treated | surgery (remove endocrine source) hormonal therapy (block hormone signal) |
| how can chemicals cause cancer | can generate free radicals causing DNA damage over time |
| how does smoking affect cancer | dose dependent, numerous carcinogens cessation = best prevention |
| pathogenic causes of cancer | H. Pylori HPV (rectal/oral/uterine) Hep B/C HIV |
| initiation promotion progression theory | 1. initiation (carcinogen exposure) 2. promotion (promoter influence ie inflammation/chemicals/hormones) 3. progression (malignancy) |
| autonomy | unregulated proliferation of neoplasm, nonresponsive to growth signals |
| what do neoplasms do | produce abnormal/excessive growth signals rapid cell division (compete for nutrients/starve other cells) angiogenesis |
| benign tumors, why can they still be bad | possible compression/obstruction |
| what are benign tumors | slowly growing localized, made of well-differentiated cells usually |
| local spread | keeps tumor within tissue of origin |
| direct extension | invade adjacent tissue/organ |
| metastasis | lymph/vascular system spread to distant sites |
| seeding | cancer cells disseminate from a primary tumor to distant sites in the body, and may also return to the primary tumor occurs in body cavities |
| organ tropism | preference to migrate to specific organs |
| -oma | indicates tumor |
| carcinoma | malignant EPITHELIAL tumors |
| sarcoma | malignant CONNECTIVE TISSUE tumors |
| carcinoma in situ | malignant epithelial cells not yet beyond basement membrane |
| rhabdomyoma/rhabdomyosarcoma | striated muscle cell tumor |
| leiomyoma/leiomyosarcoma | smooth muscle cell tumor |
| chondroma/chondrosarcoma | cartilage tumor |
| cancer staging | higher stage # = bigger size/progression (stage I-IV) |
| TNM | T = tumor size N = lymph node involvement M = metastasis |
| T classification | T for tumor TX = tumor cannot be evaluated T0 = no evidence of primary tumor Tis = carcinoma in situ (no spread) T1-T4 = size and extent |
| N classification | N for lymph node NX = regional lymph nodes cannot be evaluated N0 = no lymph node involvement N1-3 = involvement of lymph nodes |
| M classification | M = distant metastasis MX = cannot be evaluated M0 = no metastasis M1 = metastasis |
| what does tumor grading I-IV mean | I = well differentiated II = moderately differentiated III = poorly differentiated IV = undifferentiated |
| why is differentiation important in cancer classification | well differentiated = closer to normal tissue undifferentiated = lack of specialization/increased genetic instability |
| cancer prognosis | 5 year survival rate benchmarking depends on TNM, location, overall health and treatment response |
| ectopic hormone production | non endocrine tumors secreting hormones |
| general manifestations of tumor | lymphadenopathy unexplained fever anorexia cachexia paraneoplastic syndromes ectopic hormone production loss of tissue function |
| paraneoplastic syndrome | hormonal/neurological effects not directly caused by tumor mass |
| how does cancer cause unexplained fever | release pyrogens resulting in immune response (remember pyrexia is fever) |
| gold standard for diagnosis/confirmation of malignancy | biopsy/cytology microscopic examination of tumor cells |
| tumor markers | PSA, CEA, CA125, AFP, CA 19-9, hCG, calcitonin, catecholamines |
| what lab tests can be done to check for cancer | tumor markers, CBC, liver function test |
| cancer treatments | surgery, chemotherapy, radiation, hormonal therapy, immunotherapy |
| radiation therapy | localized high energy waves/particles damage cancer cell DNA |
| chemotherapy | systemic agents targeting cancer cells |
| immunotherapy | immune system to combat cancer immune checkpoint inhibitor/monoclonal Ab/CAR T-cell therapy |
| children and cancer | childhood cancers usually originate in ectodermal and mesodermal germ layers |
| ectodermal | (skin) nervous system in embryonic development |
| mesodermal | muscle/bones in embryonic development |
| clinical signs of childhood cancer | nonspecific usually persistent fatigue, bone pain, weight loss |
| NSCLC | non small cell lung cancer 95% adenocarcinoma, squamous cells/large cells |
| SCLC | small cell lung cancer 15% highly malignant often metastatic |
| clinical manifestations of lung cancer | cough, hemoptysis, chest pain, dyspnea fatigue, weight loss and potential paraneoplastic syndrome |
| paraneoplastic syndromes | disorders caused by cancer due to immune response ie. SIADH in lung cancer |
| lung cancer diagnosis | CXR/CT bronchoscopy, sputum cytology, tissue biopsy TNM staging |
| lung cancer treatment | surgery (wedge resection) chemo and radiation combo (especially for SCLC) targeted therapy for specific mutations |
| colon cancer | most common GI tract CA usually seen in age 50+ |
| risk factors for colon CA | FHx, chronic IBD, high fat, low fiber, smoking, EtOH |
| pathophysiology of colon CA | adenomatous polyps -> dysplasia -> adenocarcinoma |
| common mutations of colon CA | APC, KRAS, p53 chromosomal instability or replication error |
| clinical manifestation of colon CA | early stage = asymptomatic occult stool, altered BMs, anemia, abdominal pain |
| diagnosis of colon CA | colonoscopy, FOBT, cologuard, stool guaiac, biopsy imaging |
| treatment for colon CA | resection (curative if localized) chemotherapy and/or radiation for advanced |
| colon CA prognosis | 90%/5 years for early significant decline in prognosis if metastatic |
| brain CA | often metastatic (lung, breast, melanoma) |
| primary brain CA | glioma, meningiomas, pituitary adenomas |
| brain CA in children vs adults | children = cerebellar adults = cerebral |
| gliomas | glial cell origin, benign/malignant type |
| pathophysiology of brain CA | increased ICP (cause headache, vomiting, hernation) does not usually metastasize beyond CNS |
| clinical manifestation of brain CA | headache (worse in morning) vomiting seizure focal neuro deficits (weakness/numbness/visual change/speech deficit) |
| diagnostic criteria for brain CA | neuro exam (reflex/cranial nerve/motor sensory function) imaging (MRI/CT) biopsy if accessible |
| what classification system used for brain CA | WHO classification, does not use TNM classification |
| treatment for brain CA | surgery (if resectable) radiation chemotherapy (intrathecal -> in the spinal canal/subarachnoid space) palliative measures (manage edema/seizure/pain) |
| leukemia | over production of immature/abnormal WBC (malignant disorder of blood forming organ) |
| types of leukemia | acute vs chronic lymphocytic vs myelogenous (cell lineage) speed of onset |
| myeloid | stem cells that turn into blood cells/WBC |
| acute lymphocytic leukemia found in age | most common childhood cancer |
| acute myeloid leukemia found in age | more common in adults |
| pathophysiology of acute leukemia | excessive -blasts (lymphoblast vs myeloblasts) crowd out normal RBC/platelets leading to anemia, thrombocytopenia and infection |
| clinical manifestation of acute leukemia | increased infection fever pallor/fatigue (anemia) bruising/bleeding (thrombocytopenia) headache/vomiting (CNS involvement esp in ALL) |
| diagnostic criteria of acute leukemia | elevated blasts (>20%) in CBC bone marrow bx cytogenic analysis |
| treatment for acute leukemia | combination chemo intrathecal chemo with/without cranial radiation (for ALL) bone marrow/stem cell transplant |
| autologous transplant | stem cell transplant from self |
| allogenic transplant | stem cell transplant from donor |
| when is stem cell/bone marrow transplant considered in acute leukemia | for high risk, relapsed or refractory ALL/AML |
| refractory ALL/AML | acute leukemia that does not respond to initial treatment w/o complete remission |
| chronic lymphocytic leukemia (CLL) characteristics | usually in older adults abnormal B lymphocytes |
| chronic myelogenous leukemia (CML) characterized by? | philadelphia chromasome |
| CLL pathophysiology | hypoproliferative but nonfunctional B-cell accumulates |
| CML pathology | excess granulocyte, RBC and platelet with altered differentiation remember myeloid = blood cell progenitor |
| clinical manifestation of CLL/CML | early stage often asymptomatic, usually found on CBC fatigue, infections, splenomegaly, low grade fever, weight loss |
| diagnostic criteria for CLL/CML | elevated WBC count bone marrow bx philadelphia chromosome detection |
| CLL treatment | no treatment until symptomatic, then chemotherapy |
| CML treatment | tyrosine kinase inhibitors or possible transplant bone marrow transplants are not common in chronic leukemia |
| major type of lymphoma | hodgekin lymphoma (HL) non hodgekin lymphoma (NHL) |
| reed-sternberg (RS) cells | present in hodgekin lymphoma, not present in non hodgekin lymphoma basically giant abnormal lymphocyte usually derived from B-lymphocytes |
| lympohoma | malignant lymphocytes forming solid tumor in lymph tissue |
| hodgekin lymphoma characteristics | RS cells bimodal age distribution from 10-30 and >50 |
| hodgekin lymphoma pathophysiology | RS secrete cytokines -> infiltration of inflammatory cells in lymph nodes usually start in one node (cervicals) and spread continuously possible link to EBV |
| clinical manifestations of hodgekin lymphoma | painless lymph node enlargement B symptoms (fever, night sweat, weight loss, itchy skin) mediastinal mass, splenomegaly, hepatomegaly |
| HL diagnostic criteria | RS cells confirm dx Ann Harbor staging |
| Ann Arbor staging | similar staging to TNM (also from 1-4) for lymphoma |
| treatment for HL | - chemo with/without radiation - stem cell transplant in refractory/relapsed 85% survival rate |
| nonhodgekin lymphoma chracteristics | broad category of B-cell (85%) or T-cell (15%) malignancy NO RS cells MULTIPLE lymph node involvement |
| whats different between HL and NHL? | presence of RS cells single lymph node initial involvement (HL) vs multiple lymph node involvement (NHL) |
| NHL pathophysiology | genetic mutation in protooncogenes or tumor suppressor genes non contiguous lymph node involvement = possible spread to spleen, liver and bone marrow |
| NHL clinical manifestations | painless lymph node enlargement (possibly more than 1) fever, night sweat, weight loss (similar to HL) possible paraneoplastic syndrome and immunodeficiency |
| NHL diagnostic criteria | lymph node bx and histologic classification imaging (CT/PET) staging (1-4) |
| subtype of NHL | indolent vs aggressive subtype |
| NHL treatment | dependent of NHL subtype combination chemotherapy/radiation and immunotherapy stem cell transplant in high risk/relapse |
Created by:
sleepingbear
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