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LIPID ABNORMALITIES

Physiology of lipid metabolism • Triglycerides (Tg), cholesterol (both free and esterified), free fatty acids (FFA) and phospholipids (Pl) constitute the plasma lipids. • Lipoproteins are complexes of lipids and proteins that are essential for the transport of cholesterol, triglycerides, and fat-soluble itamins • !on-polar lipids(insoluble in "ater) li#e triglycerides (Tg) and cholesterol esters form the core "hile Pl and free cholesterol along "ith certain specific proteins called apoproteins (Apo) constitute $lipoproteins% (Lp). • The lipoproteins ha e been classified into four ma&or classes, chylomicron ('m), ery lo" density lipoprotein ((L)L), lo" density lipoprotein (L)L) and high density lipoprotein (*)L). *)L is the smallest in si+e and (L)L is largest in si+e.

Apolipoproteins maintain structure of arious lipid particles and also help in their metabolism. ,.g -.//, - 01. LIPID-LIPOPROTEIN METABOLISM a) E oge!o"s lipid t#a!spo#t • )ietary fat and cholesterol are incorporated into chylomicron, in the intestinal epithelial cells along "ith specific apoprotein. • The 'm is then released into the lacteals and through the cisterna chyla-thoracic duct system enters into the circulation. • At the capillary- tissue interface the en+yme LPL catalyses the brea#do"n of chylomicron and causes liberation of FFA and monoglycerides. • The FFA is utilised for energy purposes or resynthesis of Tg in the adipose tissue "hile glycerol reaches the li er to be utilised for endogenous triglycerides synthesis. E!doge!o"s lipid t#a!spo#t

The circulation and metabolism of (L)L molecules constitute the endogenous lipid transport. (L)L "ith shedding of the Tg load. &lassifi%atio!' .. Re$e#se %holeste#ol t#a!spo#t • *)L secreted from the li er and gut.L)L is ery rich in cholesterol and most atherogenic. "hile some gets con erted into bile acids and is then secreted so as to help in fat absorption from the gut.• 'holesterol deri ed from exogenous lipid transport or synthesised by the li er • • • • from non-cholesterol sources has three different fates. The rest is incorporated into (L)L for transportation and distribution to different tissues. a process "hich is re erse to both endogenous and exogenous lipid transport and so is called 5re erse cholesterol transport5. 2ome is secreted into the gut as such. Predominant hypertriglyceridaemia . • *)L "hile interacting "ith peripheral tissue ac4uire cholesterol. Predominant hypercholesterolaemia 6. *)L is rich in Apo A. 3)L is further metaboli+ed to L)L( lo" density lipoprotein) L)L is the end-product of (L)L metabolism. • !et result is *)L is engaged in mobilising cholesterol from peripheral tissues to li er. the (L)L becomes smaller and less compact "ith cholesterol content becoming intermediate-density lipoprotein (3)L).this done in presence of en+yme L'AT ( lecithin cholesterol acyl transferase).

&li!i%al feat"#es' • Asymtomatic. of 1*rs). • . in LPL deficiency patients. T=. corticosteroids • )rugs (. This should include 9 Total cholesterol. familial hypertriglyceridemia. 8ixed *yperlipidaemia 9 both cholesterol and triglycerides are increased • Fredric#son classification is ery complicated.deposits around eye esp. *T! or 'A). I!$estigatio!s' • 2erum lipids should be as#ed on fasting (min. TFT. • Any patient "ho has presented "ith early onset of 'A) suspect familial lipid abnormalities.7. urine protein. • Patient may present "ith pancreatitis esp. BFT. LFT. • <anthomas 9 on Achilles tendon. platella and bac# of hand. C As# for drug history li#e beta-bloc#ers. • > L)L cholesterol ? Total cholesterol-(*)L @T=A:) • secondary causes of dyslipidemia ha e to be ruled out 9 sugars. upper eye lid. and accidentally detected due e aluation of )8.xcess alcohol retinoids. • <antholesma -.rupti e <anthomas 9 o er buttoc#s seen esp.-bloc#ers. • 8ost of the signs gi en abo e are more common in familial ariants than secondary causes. • 'orneal arcus. 3n this classification di ided lipid abnormalities into : groups.L)L cholestrerol. P#ima#y %a"ses Se%o!da#y &a"ses • *ypothyroidism Etiology Type (ype#%holeste#olaemi a • Familial hypercholesterolaemia • *yperalphalipoproteinaemia (ype#t#igly%e#idaemia • Lipoprotein lipase deficiency • Familial hypertriglyceridaemia • • • • • !ephrotic syndrome 'hronic li er disease )iabetes mellitus 'ushing%s syndrome )iabetes mellitus (type 6) • 'hronic renal disease • . *)L. .

E. encouragement and other measures should be underta#en to reinforce patient compliance B) Pha#ma%ologi%al t#eatme!t Lipid ab!o#mality *ypercholesterolemia *ypertriglyceridemia Mi ed (ype#lipidaemia D#"g of %hoi%e 2tatins Fibrates 2tatins @ Fibrates (M) &o Red"%tase I!hibito#s *stati!s) • E+g 2ima astatin (:-.E.3 9 se ere renal and hepatic dysfunction. A) Dieta#y a!d life-style • This is the cornerstone of therapy in the management of hyperlipidaemias.A 9 3nhibits cholesterol synthesis.g 9 'holestyramine and cholestipol. -en+afibrate. legumes. • 8. • 2ide effects 9 8yositis.g =emfibrocil. fruit.A 9 Anion exchange resins.3 9 pregnancy and lactation and li er disorders. • Deight reduction and maintenance of near normal body "eight is desirable esp for • • • hypertriglyceridemia./ per cent of daily calorie re4uirement. • '. . 8yositis. dietary fibre and plant sterols Besponse to diet is usually apparent "ithin 7-0 "ee#s. • 8.E./mg). 2upplementary inta#e of foods containing lipid-lo"ering nutrients such as n-7 fatty acids. • 2ide effects 9 increase in li er en+ymes./mg) Ator astatin (:-. &holeste#ol Bi!di!g #esi!s' • .. • 8. • • . finofibrate. pulses. The lipid-lo"ering diet should aim at reducing the total fat inta#e to 7/ per cent along "ith reduction of saturated fat to less than .Ma!ageme!t' • Lipid-lo"ering therapies ha e a #ey role in the secondary and primary pre ention of cardio ascular diseases. fish.A 9 decrease the hepatic triglyceride synthesis. unrefined carbohydrates. . 3ncrease consumption of cardioprotecti e and nutrient-dense foods such as egetables.ib#i% a%id de#i$ati$es' • .. nausea and impotence.xplanation. • '.

E. abnormal LFT. Omega .• 2ide effects 9 nausea and flatulence and abdominal bloating.icosapentaenoic acid (. &holeste#ol abso#ptio! i!hibito#s.A 9 .g -e+etimibe These inhibit the intestinal mucosal transporter that absorbs dietary and biliary cholesterol. 'H and li er function ha e to be regularly assessed. Ni%oti!i% a%id de#i$ati$es' • 8. . breast-feeding. • '. Mo!ito#i!g of the#apy The effect of drug therapy can be assessed after G "ee#s. 2o generally used in combination "ith statins.fatty a%ids*fish oils)' • 8. rashes.PA and )*A are potent inhibitors of (L)L T= formation.PA) and docosahexaenoic acid ()*A) comprise approximately 7/F of the fatty acids in fish oil.3 9 pregnancy.E..A 9 inhibit lipid synthesis in the li er. • 2ide effects 9 nausea and belching. . • 2ide effects 9 headache. 8echanism of action is synergistic "ith the effect of statins.

'hol-*)L) J.7/ J. mg/dL Primary TargetI L)L 'holesterol J.7/ J. ris# factor .G/ J.// J.G/ 2econdary TargetI !on-*)L 'holesterolC (T.L/ 'A) and 'A) ris# e4ui alentsC 8ultiple (6@) ris# factors Kero to .Ta#get $al"es of lipids The#ape"ti% )oal.

diabetes . abdominal aortic aneurysm.Cclinical forms of non-coronary atherosclerotic ascular disease (peripheral arterial disease. clinical carotid artery disease).