liquid part of the blood, or plasma, is separated from the blood cells. Typically, the plasma is replaced with another solution--> returned to body

degree of abnormality of APC-assay correlates to heterozygosity (higher APC ratio) or homozygosity (low APC ratio) factor V Leiden mutation

LMNA codes for Lamina A-protein that acts as scaffolding on the inner side of the nucleus->farnesyl stays on lamina A->piles on=abnormal nuclear envelop

BRCA2: tumor suppressor, chromosome stability; BRCA1: tumor suppressor,DNA damage response/repair; HER2: proto-oncogene, nonregulated tissue growth

TTP->ADAMTS13 deficient->cleavage down, increase vWG multimers->hypercoagubale->prothombotic->aggregate->obstruct vessel->sheering RBCS=shistocytes

Inactive (parent drug)-> metabolized-> metabolites FdUMP block TS=interfere with DNA/RNA/protein formation

HUS: shiga toxin->ADAMTS 13 inhibition->failure to cleave vWF multimers; TTP: ADAMTS13 antibodies/congenital ADAMTS13 mutation->failure to cleave vWF multimers

genetics (BRCA1/2, HER2); Demographics (female, older); prolonged estrogen exposure; Previous cancers/radiation; Lifestyle (alcohol, BMI, smoking)

immune cells trigger inflammation->cytokines->inflammatory markers->activate nociceptors throughout body

Purpura, Confusion, Arrhythmia, Proeinuria, increase serum indirect bilirubin + LDH, decrease haptoglobin

LDH: high turn over of cells-excess cell lysis; Uric Acid-breakdown of cellular nucleic acid contents of leukemia cells

1. Warfarin-block carboxylation of prothrombin/VII/X & proteins C/S->deactivates Vitamin K; 2. Dabigatran-inhibit thrombin; 3. Rivaroxaban-direct Xa inhibitor

T: extent/size of tumor (how far grown in wall colon-mucosa, muscularis properia, suberosa/serosa); N: spread to nearby lymphs; M: metastasis to distant organs