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110 Cards in this Set
- Front
- Back
Apoptosis is characterized by what cell changes
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cell shrinkage, nuclear shrinkage (pyknosis), basophilia, membrane blebbing, nuclear fragmentation (karyorrhexis), forming apoptotic bodies
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Apoptosis: Intrinsic pathway
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involved in tissue remodeling, embryogenesis. Growth factor is withdrawn from proliferating cells: ↑ Bax ↓ Bcl-2 -> Cytochrome C -> Cytosolic caspases
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Apoptosis: Extrinsic pathway (2 pathways)
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1) Fas-L binding Fas 2) Cytotoxic T cell releases Granzyme B & Perforin
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CD95 =
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Fas-Receptor
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Coagulative necrosis
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heart, liver, kidney
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Liquefactive necrosis
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brain, abscess, pleural effusion
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Caseous necrosis
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TB, systemic fungi
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Fatty necrosis
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saponification, peripancreatic fat
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Fibrinoid necrosis
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BVs
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Gangrenous necrosis 1) dry 2) wet
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1) dry ischemic coagulative 2) wet has bacteria. Limbs & GI tract
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Reversible cell injury
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↓ ATP, cellular swelling, nuclear chromatin clumping, ribosomal detachment, ↓glycogen, fatty change
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Irreversible cell injury
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Ca++ influx activates caspases, PM damage, Mitochondrial permeability, lysosome rupture, nuclear pyknosis, karyolysis, karryorhexis
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Hypoxia in brain
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ACA/MCA/PCA watershed
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Hypoxia in heart
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subendocardium of LV
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Hypoxia in kidney
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straight segment of PT (medulla), TAL (medulla)
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Hypoxia in Liver
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zone III (around central vein)
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Hypoxia in colon
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splenic flexure, rectum
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Hypoxic ischemic encephalopathy affects
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pyramidal cells of hippocampus & purkinje cells
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Red infarct
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hemorrhagic. Red = reperfusion injury. Loose tissues with collaterals. (liver, lung, intestine)
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Pale infarct
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ischemia: solid tissues with single blood supply: heart, kidney, spleen
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↑ TPR, low CO, cold, clammy patient = what kind of shock?
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hypovolemic
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↓ TPR, dilated arterioles, high VR, hot patient = what kind of shock?
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septic
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Acute inflammation
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neutrophils, eosinophils, antibodies. Rapid. Abscess.
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Chronic inflammation
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mononuclear cells: persistent destruction & repair. BV proliferation & fibrosis: Scar, amyloidosis
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Granuloma
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nodular collections of epithelioid macrophages and giant cells.
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Leukocyte rolling
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E&P selectin + Sialyl Lewis
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Leukocyte tight binding
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ICAM-1 & integrin (LFA-1)
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Leukocyte diapedesis
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PECAM1
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Leukocyte migration
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C5a, IL-8, LTB4, Kallikrein
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Mechanism of injury caused by carbon tetrachloride?
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Free radical injury -> necrosis & fatty change
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Free radical pathologies
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Retinopathy of prematurity, bronchopulmonary dysplasia, CCL4, Acetaminophen overdose, hemochromatosis, repurfusion after anoxia
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Free radicals eliminated by what enzymes
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superoxide dismutase, catalase, glutathione peroxidase
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antioxidant vitamins
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A, C, E
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Wound healing: INFLAMMATORY STAGE
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Plts, NΦ, MΦs: Clot, vessel perm, NΦ migration, MΦ clear debris
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Wound healing: PROLIFERATIVE STAGE
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Day 2-3. Fibroblasts, myofbs, endoth cells, keratinocytes, MΦs. GT & Collagen, angiogenesis, epith cell proliferation, clot dissolution, WOUND CONTRACTION
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Wound healing: REMODELING STAGE
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FIBROBLASTS: Replace Type III collagen with Type I collagen for tensile strength
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wound contraction mediated by
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myofibroblasts
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Cells that mediate granuloma formation
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Th1 secrete gammaINF -> Macrophages -> TNFa
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Specific gravity of transudate vs exudate
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transudate < 1.012, exudate > 1.012
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cellularity & protein content of transudate vs exudate
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transudate: hypocellular, protein poor exudate: hypercellular, protein rich
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Transudate caused by:
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↑ hydrostatic P ↓ oncotic P, Na+ retention
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Exudate caused by:
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lymphatic obstruction & inflammation
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ESR
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when aggregated from products of inflammation coating RBCs, they fall at a faster rate in the test tube
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↑ESR
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infection, inflammation, cancer, pregnancy SLE
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↓ESR
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Sickle cell (altered shape), Polycythemia (too many), CHF (who the hell knows)
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Cell death by peroxidation of membrane lipids from poisoning by:
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Iron
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Waxy appearance due to beta pleated sheet structure aggregations:
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amyloidosis (oh ya and apple green birefringence)
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Primary amyloidosis due to what protein
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AL = Ig Light chain deposits. Plasma cell disorder or multiple myeloma
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Secondary amyloidosis due to what protein
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AA = Fibrils of serum Amyloid A. Chronic diseases like RA, IBD, spondyloarthropathy, chronic infections
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Dialysis related amyloidosis
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beta2microglobulin fibrils. Presents as carpal tunnel syndrome
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Heritable amyloidosis
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Transthyretin gene mutation -> ATTR neuro/cardiac amyloidosis
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Age related amyloidosis
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deposition of normal TTR in myocardium
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Organ specific amyloidosis
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ex: APP into amyloid beta in Alzheimers
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Metalloproteinases secreted by cancer cells indicate they are now:
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INVADING
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Metaplasia
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One adult cell type replaced by another
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Dysplasia
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abnormal growth with loss of orientation size and shape compared to normal tissue
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Anaplasia
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abnormal cells lacking differentiation: primitive cells of same tissue
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Neoplasia
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clonal proliferation of cells, excessive, uncontrolled
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desmoplasia
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fibrous tissue formation in response to neoplasm
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Tumor Grade
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Degree of differentiation
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Tumor Stage
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Stage = Spread
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Cachexia mediated by
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TNFalpha, INFgamma, IL-6
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Tyrosine Kinase oncogenes:
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"though still ABLe, ERB was Tyred, so he RETired" abl, c-erbB2 (HER2neu), ret
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abl
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CML, tyrosine kinase
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HER2/neu
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breast, ovarian, gastric, tyrosine kinase
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Ret
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MEN 2A & 2B (Tyrosine kinase)
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Transcription factor oncogenes
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"mycs" c-myc, l-myc, n-myc
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c-myc
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burkitt's..duh. TF
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L-myc
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L=Lung tumor. TF
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N-myc
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N=Neuroblastoma. TF
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bcl2
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antiapoptotic oncogene, follicular lymphoma
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Ras
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oncogene: colon CA (GTPase)
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c-kit
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Gastrointestinal stromal tumor (GIST), CytoKIe receptor oncogene
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Rb
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RetinoBlastoma, osteosarcoma. Rb = chrom 13. Inhibits E2F GI->S phase
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p53
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TSG. Li fraumeni syndrome (17p), TF for p21
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BRCA1, BRCA 2
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TSG: breast & ovarian cancer. DNA repair proteins [chrom 17, 13]
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p16 & BRAF
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melanoma
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APC
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TSG: coloectal cancer. Polyp = 5 letters, chrom 5
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WT1
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TSG: wilm's tumor (nephroblastoma)chrom 11
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NF1
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NF type 1, TSG, chrom 17. RAS GTPase activating protein
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NF2
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NF type 2, Chrom 22, merlin schwannomin protein
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DPC4
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TSG: "Deleted in Pancreatic Cancer"
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DCC
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TSG: "Deleted in Colon Cancer"
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CEA
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CarcinoEmbryonic Antigen. Colorectal and pancreatic cancers
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alphaFP
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HCC, GCTs
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CA-125
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Ovarian cancer
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s100
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melanoma, neural, schwannomas
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alkaline phosphatase
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mets to bone, liver, paget's
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calcitonin
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medullary thyroid carcinoma
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keratin+
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epithelial surfaces
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Aflatoxin
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HCC
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vinyl chloride
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liver, angiosarcoma
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CCL4
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liver, fatty change, centrilobular necrosis
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Nitrosamines
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gastric cancer
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cigarette smoke LAWL
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SCC of larynx, lung, small cell, RCC, transitional cell, pancreatic
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Asbestos
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bronchogenic CA > mesothelioma!!!
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arsenic
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SCC skin Angiosarcoma of liver
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Naphthalene (aniline) dyes
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Transitional cell carcinoma (bladder)
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aklylating agents
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leukemia
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PSaMMoma bodies
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papillary (thyroid) Serous (ovary) meningioma mesothelioma
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male cancer incidence
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prostate > lung > colon
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male cancer mortality
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lung > prostate
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female cancer incidence
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breast > lung > colon
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female cancer mortality
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lung > breast
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ACTH or ACTH like peptide Paraneoplastic syndrome
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cushing's syndrome effect. Small cell
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paraneoplastic syndrome: ADH
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SIADH effect from small cell lung carcinoma & intracranial neoplasms
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paraneoplastic syndrome: PTHrP
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hypercalcemia. Squamous cell lung CA, RCC, breast
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paraneoplastic syndrome: calcitriol
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hypercalcemia. Hodgkins
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paraneoplastic syndrome: EPO
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polycythemia effect from RCC, hemangioblastoma, HCC, pheochromocytoma
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paraneoplastic syndrome: antibodies against presynaptic Ca++
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lambert eaton syndrome, small cell
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