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

Proteins S & C work together to prevent your blood from clotting too much; if low S&C = clot too much; P&C inactivate factors V/VIII = slow down clot formation

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

glucose-6-phosphatase deficiency (can't go from G6P to Glucose)

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

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

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

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

1.primary hemostasis- PLT adhesion; 2.secondary hemostasis- vWF complexes VIII->prolong half-life VIII (prevent its degradation)->complex IX->activate X

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