BioChem Exam 3 Practice Questions with verified answers, Exams of Nursing

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BioChem Exam 3 Practice Questions

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Structure and biophysical properties of complex lipids (glycerophospholipids vs. sphingolipids) - correct answer ✔✔Biophysical property of sphingolipid (detergent resistant) compared to glycerophospholipid (detergent soluble) Three components of glycerophospholipids - correct answer ✔✔(1) glycerol backbone; (2) fatty acid chains at sn-1 and sn-2 position; (3) phospho-head group (choline, ethanolamine, serine, glycerol). Cardiolipin is a special glycerophospholipid which has shared glycerol as head group Glycerophospholipids synthesis: de novo pathway or remodeling pathway. - correct answer ✔✔In remodeling pathway, the head groups of phosphatidylcholines (PC), phosphatidylserine (PS), and phosphatidylethanolamine (PE) can be interconverted into each other; the fatty acid chains can be switched between different glycerophospholipids by acyltransferase Role of phospholipase? - correct answer ✔✔Glycerophospholipids are metabolized by phospholipases PLA1/2 and release fatty acid, for example, PLA2 releases AA for COX pathway. Phosphors head group can be released by PLC. For example: PLC hydrolyzes PIP2 to release IP3 that triggers calcium and also produces DAG that activates PKC pathway. PLC can also release GPI-anchored protein from GPI-anchor. Three components of sphingolipid - correct answer ✔✔ (1) sphingosine backbone (2) fatty acid chain (3) head group (H for ceramide; phosphocholine for sphingomyelin; sugars for glycosphingolipids) Which sphingolipid plays a central role in sphingolipid metabolism? - correct answer ✔✔Ceramide can be de novo synthesized and it is the precursor for all other sphingolipids. Ceramide is mainly from de novo synthesis or metabolized from either sphingomyelin or glycosphingolipids What are gangliosides and their function? - correct answer ✔✔Gangliosides are glycosphingolipids with a polysaccharide chain, which contains sialic acid. The polysaccharide chain of gangliosides can serve as receptor for bacterial proteins: for example, cholera toxin binds to ganglioside GM

Sphingolipid metabolism - correct answer ✔✔Sphingolipids are primarily degraded in lysosomes by lysosomal hydrolases. Deficiency in a certain lysosomal hydrolase activity results in accumulation of precursor for this hydrolase in lysosomes causing lysosome storage diseases. Describe Gaucher disease, an example of lysosome storage disease. - correct answer ✔✔Deficiency in glucosidase, a lysosomal hydrolase hydrolyzes glucosylceramide in ceramide, causes accumulation of glucosylceramide in lysosomes leading to Gaucher disease The primary source of each lipoprotein particles? - correct answer ✔✔The source of each lipoproteins: chylomicron in the intestine, VLDL and HDL in the liver. IDL and LDL are derived from VLDL by lipase. The relative content of triglycerides and cholesterol in lipoprotein particles - correct answer ✔✔Chylomicron: highest in triglycerides LDL: highest in CE. The structural role of apolipoproteins? - correct answer ✔✔Apolipoproteins: structural role, required for de novo synthesis (ApoB48 for chylomicron; ApoB100 for VLDL, IDL, LDL; ApoA for HDL). Chylomicron, VLDL, HDL are de novo synthesized. IDL and LDL are derived from VLDL. Relative lifetime of each lipoprotein particle. - correct answer ✔✔HDL>LDL>VLDL>Chylomicron

• Both ApoB100 and ApoE are ligands for LDLR. However, ApoB100 has lower affinity to LDLR compared to ApoE. Chylomicron and VLDL have both ApoB and ApoE. The triglycerides in chylomicron and VLDL are rapidly hydrolyzed by LPL and the chylomicron remnants and VLDL remnants are cleared by liver through LDLR and LRP. LDL has only ApoB100 but not ApoE. HDL has ApoA but not ApoB100 or ApoE. HDL does not bind to LDLR Lipoprotein receptors and their function? - correct answer ✔✔LDLR is regulated by intracellular cholesterol. Scavenger receptor is not regulated by intracellular cholesterol. Foam cell formation is due to continuously uptaking of oxidized LDL via scavenger receptor. Function of lipase? - correct answer ✔✔(1) Lipoprotein lipase (LPL) converts chylomicron to chylomicron remnant and also converts VLDL to VLDL remnant (IDL) (2) HTGL converts VLDL remnants (IDL) to LDL

Acyltransferase - correct answer ✔✔(1) LCAT in HDL converts free cholesterol to CE (2) ACAT inside cells converts free cholesterol to CE and CE is stored in lipid droplets Transporter - correct answer ✔✔(1) ABCA1 transports free cholesterol from cells to HDL (2) CETP transfers CE from HDL to triglyceride-rich lipoproteins (chylomicron, VLDL, or their remnants) in the exchange of triglyceride Lipoprotein transport pathways - correct answer ✔✔(1) fuel transport (2) overflow (3) reverse cholesterol transport. Lipoproteins in fuel transport pathway? - correct answer ✔✔Chylomicron and VLDL are the lipoproteins in fuel transport pathway in feed or fast situation, respectively. Notice the different lipoprotein substrate of LPL and HTGL Lipoprotein in overflow pathway? - correct answer ✔✔LDLR is controlled by intracellular cholesterol synthesis. High level of intracellular cholesterol (1) downregulates LDLR, decreased LDL intake (2) downregulates HMG-CoA reductase, decreased cholesterol de novo synthesis (3) upregulates ABCA1, increased cholesterol export Lipoprotein in reverse transport pathway? - correct answer ✔✔HDL. Understand the role of ABCA1, LCAT, CETP. Genetic and environment factors lead to hypercholesterolemia - correct answer ✔✔Understand ApoB100 overproduction, ApoE deficiency, LDLR deficiency The basic process in the development of atherosclerotic plaque (atherogenesis)? - correct answer ✔✔The early events include endothelial dysfunction, inflammation, monocyte transmigration, lipid deposition (foam cell), smooth muscle cell migration and proliferation. The late events are fibrotic plaque formation and plaque rupture leads to atherothrombosis

Treatment of dyslipidemia? - correct answer ✔✔Statins, PCSK9 inhibitor etc. PCSK9 inhibitor increases LDLR expression and cholesterol uptake, thereby decreases plasma LDL level What is a thrombus and its physiological/pathological roles? - correct answer ✔✔a. Hemostasis is to stop bleeding by forming a plug (thrombus) at the site of vascular injury b. Aggregated platelets that form a platelet plug stabilized by cross-linked fibrin protein c. Thrombosis can block the diseased or healthy blood vessels Describe the events following endothelial damage in hemostasis: - correct answer ✔✔- damaged endothelial cells release factors (vWF/PAF) and subendothelial collagen exposure trigger platelet activation, adhesion and aggregation

• activated platelets release vasoconstrictors (serotonin, TXA2) to limit blood flow to the area of injury The major anti-platelet factors produced by endothelial cells? - correct answer ✔✔Prostacyclin (PGI2) and nitric oxide are potent vasodilator and plate inhibitor produced by healthy endothelial cells. What is the role of TXA2 in platelet activation? - correct answer ✔✔- Many platelet activating factors increase PLA2 activity and AA release, leading to TXA2 production
• TXA2 is a potent vasoconstrictor and a platelet activator
• TXA2 also stimulate release of ADP, a potent platelet activator, resulting in feed forward loop Pharmacology of antiplatelet drug? - correct answer ✔✔(1) block ADP receptor signaling (2) enhance cAMP singling (3) Inhibition of TXA2 production or action (aspirin) (4) GPIIb-IIa antagonists blocks platelet aggregation Difference between intrinsic and extrinsic pathway? Initiator for each pathway? Which pathway is faster?
• correct answer ✔✔- Difference: requirement for tissue factor
• Initiator (1) intrinsic pathway: surface factor XII; (2) extrinsic pathway: tissue factor (TF)
• Both intrinsic and extrinsic lead to Xa. But extrinsic is faster as it directly activates Xa. Intrinsic needs more steps to activate Xa

• Xa leads to activation of thrombin, the master regulator of coagulation o Thrombin can activate platelets by releasing TXA o Thrombin cleaves fibrinogen to fibrin, promotes fibrin crosslinking to form stabilized platelet plug o Thrombin can activate anti-coagulative protein C system The causes for prolonged APTT, PT, TCT? - correct answer ✔✔Assesses intrinsic (APTT), extrinsic (PT), final common pathway (TCT). Liver disease, vitamin K deficiency, etc. What are the three endogenous anti-coagulation systems? - correct answer ✔✔Anti-thrombin; TFPI; Protein C system What are the four groups of anti-coagulation drugs? - correct answer ✔✔ What is the role of plasmin in fibrinolysis? - correct answer ✔✔Plasminogen is the inactive pro-enzyme of plasmin. Plasminogen activator: tPA, uPA, and bacterial streptokinase. Plasmin dissolves fibrin in the blood clots, a process known as fibrinolysis. Because plasmin promotes fibrinolysis, plasmin is anti- thrombotic. PA is inhibited by PAI-1. Free plasmin is blocked by anti-plasmin. Therefore, PAI-1 and anti- plasmin are pro-thrombotic Warfarin can be used as an anti-coagulation drug. Please explain? - correct answer ✔✔Warfarin inhibits Vitamin K and then Vitamin K-dependent coagulation factor synthesis. Can we used warfarin for acute coronary syndrome and why? If not, what you suggest to use. No, it takes days for warfarin to be effective. Instead, use recombinant tPA, streptokinase to directly activate plasminogen to plasmin, which reduces coagulation by promoting fibrinolysis Structural components of a nucleotide? - correct answer ✔✔ PRPP is the precursor for the synthesis of all nucleotides both in de novo and salvage pathways. - correct answer ✔✔Overexpression of PRPP synthetase can result in overproduction of purine nucleotides leading to hyperuricemia What are the differences between de novo and salvage pathways for nucleotide biosynthesis? Which pathway is the preferred way to synthesize purine nucleotides? - correct answer ✔✔

What is the mechanism for gout symptom in Lesch-Nyhan syndrome? - correct answer ✔✔Lesch-Nyhan syndrome is an X-linked recessive disorder, which is due to HGPRT deficiency. Hypoxanthine could not be recycled to salvage pathway and leads to its accumulation. HGPRT deficiency also leads to upregulation of de novo purine synthesis. Both will increase uric acid production. The patients may have the following: hyperuricemia, gout arthritis. Gout arthritis - correct answer ✔✔Gout arthritis is mainly due to deposition of monosodium urate (uric acid in salt form) crystals in the joints, which induce inflammation and pain What are risk factors for gout development and why? - correct answer ✔✔Diet, tumor, renal disease, drug treatment, etc Treatment for gout - correct answer ✔✔Allopurinol inhibits xanthine oxidase Understand the critical role of ribonucleotide reductase (RNR) in deoxyribonucleotide biosynthesis - correct answer ✔✔Ribonucleotide reductase can reduce all ribonucleoside diphosphate (NDP) to deoxyribonucleoside diphosphate (dNDP). This enzyme is a bridge linking the RNA and DNA synthesis. Understand the effects of folate deficiency on nucleotide biosynthesis - correct answer ✔✔Folate deficiency decreases the availability of methyl donors for IMP de novo synthesis, or inhibits folate recycling thereby inhibits conversion of dUMP to TMP. Therefore, folate deficiency inhibits de novo synthesis of both purine and pyrimidine nucleotides. Understand why thymine formation pathway can be a target for cancer treatment? - correct answer ✔✔Thymine formation is unique biosynthesis pathway for TMP production. DNA synthesis is highly active in cancer cells. Blockade of thymine formation inhibits DNA synthesis without affecting ribonucleotide biosynthesis. Two enzymes of thymine formation pathway can be drug targets. (1) Thymidylate synthase: fluorocytosine (converts to FdUMP) inhibits thymidylate synthase and then TMP production (2) Dihydrofolate reductase (DHFR): inhibitors of this enzyme block folate recycling and thereby prevent TMP production