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

Type 1: partial deficiency-quantity, autosomal dominant; Type 2: qualitative variant, AD/some AR; Type 3-severe quantitative-missing vWF, Autosomal Recessive

DNA damage->lamina disrupted->chromatin conformation distress->increase p53 signaling->increase cell/tissue senescence= accelerated aging

location at the chromosome 22 breakpoint of the t(11;22)(q24;q12) translocation; EWS (EWSR1) gene is involved in translocations in Ewing's sarcoma

Factor V synthesized in liver; Thrombin activates Factor V-> prothrombin to thrombin; Factor V cofactor aPC to degrade VIII/VIIIA= reduce thrombin formation

UVB causes thymine base pairs to bind to each other->pyrimidine dimers; UVA->ROS=damage DNA repair proteins=cancer

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

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

corn starch is a glucose polymer that is broken down slowly = control glucose levels

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

Anemia -> lower oxygenation of blood->body compensates = pallor, dyspnea, tachycardia

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

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