Nst 160 Midterm 1 188 Correctly Answered Questions Latest Update

5 classes of LDL-R mutations {Ans: 1. null (no protein synthesis aka no LDL receptor) 2. transport defect (Golgi) 3. LDL binding defect 4. internalization defect (re-uptake/recycling) 5. recycling defect (can't get to cell surface)}formation of advanced, complicated lesion {Ans: -fibrous cap forms in response to injury to wall off lesion from lumen -fibrous cap covers a mixture of leukocytes, lipid and debris which may form a necrotic core -lesions expand at shoulders by means of continued leukocyte adhesion and entry -necrotic core results from apoptosis and necrosis, increased proteolytic activity and lipid accumulation}2 mechanisms that regulate AA translation {Ans: elf2 kinases, mTOR}who is more susceptible to hepatic steatosis? {Ans: hispanics 49% european-americans 23% african-americans 17%}VLDL remnant uptake {Ans: 1. remnant particle (IDL) if it contains ApoE, can be taken up by the Apo E/remnant receptor 2. increased apoCIII can impair remnant clearance 3. apoA-V another VLDL apoprotein, helps promote effective VLDL breakdown}CR may increase/decrease nicotinamide (a product and inhibitor of SIRT1 catalytic activity) {Ans: decrease}