Hyperlipidemia and Drugs Lowering Plasma Lipids - PDF
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Summary
This chapter covers hyperlipidemia and drugs used to lower plasma lipids. It describes lipoproteins, their core structure, and the various classes. The chapter also explains the different pathways of lipoprotein metabolism, including exogenous and endogenous pathways. Finally, various classifications of hyperlipidemia are also explained.
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Part 1 1: Hyp perlipide emia an nd drugs s that lo ower pla asma lip...
Part 1 1: Hyp perlipide emia an nd drugs s that lo ower pla asma lip pids █ Bas sic inform mation Lipooproteins consist off a hydroph hobic lipid d core (TGs s or cholessterol) surrounded by a hydrophilic coat of phospho olipids and d proteins (apoprotei ns), whichh render themm miscible e in aqueouus plasma. Theere are 5 classes c of lipoproteinns depend ding on the eir relative proportionn of the coree lipids, type of apop protein, sizze, and den nsity: The e intestine e is the maain source of lipid pre ecursors. The T liver i s the mainn site of syntthesis of liipoproteins s. The adi pose tissuue is the main m site o of storage of TGs. Fat cells don’tt synthesizze any lipo oproteins. ▌Lipop protein metabolis m sm In tthe exoge enous pathway, abssorbed cholesterol and a TGs aare transpoorted in plassma as chylomicro c ons. On the vascu ular endothelium, tthe core TGs is hyddrolyzed byy a surface e-bound lippoprotein lipase l into FFA whicch enter thee tissue andd utilized. The T chylom microns reemnants (c containing mainly chholesterol) pass to the liver wherre cholesterol is sto ored, oxidized to bilee acids, o or secretedd in the bile e. Alternativvely, it may y enter the e synthesiss of VLDL. In the endo ogenous pathway, p cholesterool and ne ewly synthhesized TGs T are assembled ass VLDL and delivered d to the blood wheree TGs coree is hydrolyyzed by 203 lipo oprotein lippase into FFA as d described above. The T smalleer VLDL particles p havving less TGs T and more m choleesterol are now termmed LDL. C Cholestero ol in the LDLL may be: (1) utilized by the tis sues; (2) re eturns agaain to the liiver; (3) de eposited subbintimal in blood b vess sels and ca ause atherrosclerosiis. Whe en cells diie, cholesterol in the eir plasma membrane es is returnned to the liver as plassma HDL particles. p HDL H functi ons as scaavenger lip poproteins.. ▌Class sification n of hyperlipidemiia Prim mary (fam milial; hered ditary) hyp mia: is genetically dettermined. perlipidem Class s In ncreased lipoprotein n Synonym S Type I ↑ chylomicro ons Familial chy ylomicroneemia Type IIa ↑ LDL Familial hyp percholesteerolemia IIb ↑ LDL and VLDL V Familial com mbined hyp perlipidem mia Type III ↑ IDL Familial dys sbetalipoprroteinemiaa Type IV ↑ VLDL Familial hyp pertriglycerridemia Type V ↑ VLDL and chylomicrrons Familial mix xed hyperliipedemia Sec condary (a acquired) hyperlipid demia: – Hyperchollesterolemia: hypothyyroidism, nephrotic n syndrome, s , and drugs s. – Hypertriglyyceridemia a: DM, alco ohol, gout,, chronic re enal failuree. 204