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    Metabolic Syndrome. Pharmacology. Pharmacotherapy. Pharmacy

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    Jorge Medina Fernandez
    Lecture about the metabolic Syndrome

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    Metabolic Syndrome. Pharmacology. Pharmacotherapy. Pharmacy

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    Jorge Medina Fernandez
    9 views14 pages
    Lecture about the metabolic Syndrome

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    Lecture about the metabolic Syndrome

    Copyright:

    © All Rights Reserved
    Download as PDF or read online from Scribd
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    Download as pdf
    9 views14 pages

    Metabolic Syndrome. Pharmacology. Pharmacotherapy. Pharmacy

    Uploaded by

    Jorge Medina Fernandez
    Lecture about the metabolic Syndrome

    Copyright:

    © All Rights Reserved
    Download as PDF or read online from Scribd
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    Download as pdf
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    wae Metabolic Syndrome Pharmacotherapy of Hypertension, Dyslipidemia, Obesity 15.4.2015 Metabolic Syndrome + Disesee which have affected moet ofthe world + Metabolic syndrome or Syndrome X or Reavens syndrome) isacluster of disorders with high incidence + Apr in soutal 4 persons in developed countriesone oF mare of these disorders will occur during if nl | Metabolic Syndrome 1+ Mey ia ede el po inlet eel tae kot ‘sslaeonain! snena appropiate moar te + Cina -MeatoteSatone + Indeserycommon flloving dats cold bedeeopd — 1 ipa 1 yen MetSy Definition + NCEP ATP Id. Sn patents meeting sand more oat ofthe Biase DF: shout Okey andthe Pr pet uml da 3 pg noire) ne + Sihpeniacma (neg ce > snl (sen 5 Seapetema ang 39 mt 1 SEDC weeding DLC og int capin) 2 $akdonea oy en itsmons |_Metabolic syndrome nat log) Pathophysiology Peake 3 Eeorhe n 1 Sxl iyi Go phys acy andecessatneintte) 1 Teton nclaing(Creactve pect, enone, IL, Nia + the ndincyesl te wir ft increase TNFa tere ‘stamumbsref ech: rebsonces (5: siiponecin rnin, PAL reatment Goals - Endpoints- Outcomes Max. Decraase of Total Risk = CYS morbitty and mortanty In Long-term Horizon estuction of eversibie RES: ‘smoking Dystadenia Savetes Concomten sess testmart 15.4,2015 NN ‘The heterogeneous group of Lipids covered wighenide emia hkseol phomphsiptl fe at seis vam A Be Ersnd Kclcosnoids seid hormones —~“Hypolipidemics ~ therapy of hyperlipoprot idemia oF hyperipoproteinena isthe corition of abrovmaly elevated levels of ay oa inde cet nally lvted lee of ayo all pid + Incrigheerdes, che hydra groups ofthe ghceol join ic Saliuteah unsatcbewsisetinoecens CS ee eee ica + Some cholesterol is carried asthe fe” aleool and some ‘Risk factor fr cantimasrular diseased to ther nf iScavied s fatty oy esters fered toss cholesterol + Hipolipdemicrarment slows atherosclerosis iid Taaoflesions ‘tn icp cen id fap ee ee es ‘Teaminology of lipoproteins dred fom ure: Com» ” aie Rader 8 srr zve ts om pase 5 imme esi ode ceaepyes vray tpn Sete ot eavorhreea os ees S ae ee eee i a + Soles cine eee eerste, eat camer ea power eon rem —— ‘Apoproteins + eermine plyscal chemical and immunologia certo ey emreotcal eee eres ee ine cee ea aaa ‘Sfecefroeinsand ditt tipoprottinsto ther aot Classification of hyperlipidemia Clinical importance which yp of ipids are clewated ‘lated bypscholeterolania 5 sombinsl hyptinidemin Sepiorlocaedonestatemanbeane ent According tothe tcp + coenzymesoractivators sae a eases Lecithin-cholesterol aeyltransferase (LCAT) 2 ea ey es tg rarer Lipoprotein lipase (LPL) > mixed Genetic disorders Fania hypereholesterolemia (esuency 500 ~ Htereeygs homonypoustaret) + ineased (DL “+ mutations inthe ZU gene that encase LDL tsceptar atin + bremeturecariovascua disease santhelasma 15.4.2015 Genetic disorders Fam I defeetoapo B00 Familia combined hyperlipidemia agent) + oxerpreductionotapo Bion + Ghaactersed by increased LDL cholesterol + and tighesrde concentations| Genetic disorders Familial dysbetaipoproteinemia + character by tnereaed acumulatin of VLDL remnants, LDL ghee shaleste + caused by dectne ApoE form Familial bypertrilyeeridemia ‘+ anautosomal dominanteondition (8% the population) + trigoerde levels are elevated asa rest exess hepatic production of DL neteeaypas LPL dchciney + Eeated chylomicrons in he blood Secondary disorders ypotipidemi oscars hyperthyreoss, mabye, Peru: ality. Diabetic hyperteghyeridemia typical fr both inslin epee na oeclirdepest Oi *feainacae Pg es meal lipoproteins neh fp TG Ineulficent nay ead to higher elelamsrong and VLDY, higher culating FA ncoase Re intraynthessattos + Insulin als inhibits Hormone-sensitive Lipase of at tssuethot capable of hylan Po and ease FA Secondary hyperlipoproteinemia * Hypothrteosisthe function of LDL receptor, clearance of and Diy the acti of UPL are decrease + Nephroticsyndrome ek largeamountsofptein an HDL. Hypoproesinemia stimulates protein synthesis inthe lve resting inthe overproduction of lipsprotsins (po Bio) Lipid catabolism sdereased ducto lowes levels of lipoprotein pase + Drug:concode nis bt Meche hid ie Ses hormonal contacepnes ncaa |--Secondary hyperlipoproteinemia HYPERCHOLESTEROLEMIA, ‘+ Hypothyreosis # Nephtotcsyndrome (moderate form) 2 Cholestasis 4 Drug: losposn, anticonvulsants HYPERTRIGLYCERIDEMIA, * Diabetes melitus # Chronie renal failure + Hypothyzeosis + Obesity * Alcoholism + Drugs: corticoids, retinoids, beta-blockers 15.4.2015 | tipids and atherosclerosis Secondary hyperlipoproteinemia «+ Atherosclerosis caused by thesimulaneous effet MIXED HYPERLIPIDAEMIA of high LDL, TG and low HDL = Hypotiyreosis 1 Nephrotc syndrome severe fem) ‘+ High TG alone ares ctor For pancreatitis, * Drugs thiazide like duretes, beta-Nockers + Long-term chvlomkronemi eas hepatomegaaand Increased hsemocoaguaton a ‘+ Riskof ischemic heat disease isexponenily growing with higher concentration choesteral [Pisesrtaeaae aa pathogenesi ee + Theorgnof the disease epee by the combination Upids and atherosclerosis hee + Conpllatedson 2) hppothenisof a damage of vascular endothelium jfiingemenatenst Dt pncetesi ence ela (tbo i hepa 1 Platelets acculton he pei ender lase A sedtetngaFthe wa reams by fouls pte) growth aor PDGF ace deen gro aio ta one Eipponsthe preteens soto eco terval ae ‘enact actor fom he caged enorhehumatacs aren 5 wae 5 ingnecygsthangingtemacopsagee scoop ace estar dshopettners SMES gh Ceaeoracome chino kee smog seco changes mvs all te ecamaaripn ofa el is iimacef age veri Calla sei Sere eae eats rage dee: eles, pation Hie erent hearer aed eal scene Tn oe rales atone senuagie * Smeal cold oven Lion recreate Sporn phaasehcaey | aboratory tests of lipid parameters Fee eee Pane Serena pee re «Mn esc tae elowerikthon {ngycendesand cholesterol and HL) sonic + Eoinginceeoe the cardiovascular ies + Bletrophorsis may reveal somepatholgalpoprotins sane a Dietary eine inthe fre lace Calorerstitin in obey nd eomtbateto phenotyping 1s aseat of ener saarated (nm 76 2 Ghokestermas on 5 nvr iercontont 4 Fratand vegetable gg dy (anton) 5 Elminionofescerse aloha cnsumption + Determination of apelipoprtein B, the ati oF 390 B apes + Primary dase shouldbe rete nstcondary periiemin * Pharmacotherapy the itary segment atcompaed bythe Naaman geod pee 15.4.2015 + Hyyotptients- foc hom tcton + Swinton tan cere + RARER Telecare ‘heath meta chain at + fe of heel th ernst increaed numberof satin Ebtieetpinhe ues heres rehing need pnt cin min, oe tfeieltbccmenca ont ll adr =o + Spins eduge LDL hole fesinceme HO, : oe SIS ena Sula + They neato non patets brates enfate ipoesiniensc ton ‘Snr ondeNOnceaensoeodlttion isc : = =) Tite tanned rme sean eons — sideomenincas. "ag ~ 4 Lipopilicsinvastatin lovastatin atorastatin Snatatn aio Bp er Hleophilicrsurastatin,pravestatin See ales Pharmacokinetics og auctor naan ameter dependency nf smgl dence evening ees: an ani pc om ped (Chdogznows steal sypebes shies right) nad ery eprg elon ‘+ ih binding to plana preeeins by portal ven or active transport the ver ‘+ Importance of OATP1B and P-gp transport pump 7 Stes ealand Le choletsd econ ‘sed bypecletereie. teaches an oan menhe 9 eymromePoe 1 fenmbutns res ied hppa ae 1 Rint ncarpanu nage tines h es a ae shndgianctcinntissear Sorbo see ai tpt sce . sete Seo caeegeer eae a ra Iolite tte ee cia tac contain rt Trace ctamexie pearan rrore, npn «Neji bs oon ans oeigton ries vs ontanetons 1S Tetnerdzes pagancy and esieng “a st « obo renen eee oe * omasticolfens ete aimont gece Ata Sresiona gnseglting pi and eproan aa 15.4.2015 ——— ibrates + Scimulaton of PPARsalfa by the fbrates affects pjesme aenes coding fr apo AI Ah and ‘oxidation of fay acs fala influenced + Indications: Hypertriglyceridemia, mixed EFslipidemt,Byperchoestorema + Fenofibrate - doesnot interfere with statin ‘metabolism and has lower risk of causing ‘myopathy, + is suitable to use in combination with statin | 1 Theapescenfi * Sea apetgtter=. » Seater Sera atrae acieee ea peeepreras epee nee Docs insome ygeiheendemic ree ee aes log olga hale sof cccumulaion nseere rent — Fibrates + Adverse effectstindigestion headaches, dizziness allergic shin reaction, ching: myopathy the rik slower thane Satin, rate cases to rhabdomyolyi oceasionaly increas ALT. AST, the isk of cholelithiasis (clofibrate no longer sed) + Interactions: Increases the fac of warfarin (a common blood protein binding), uriessuric gents and oral hypoglycemic agents concomitant useof statins may lead 1oinetaed risk of myopathy + Contraindcations lve: and gall ladder disease, wich ‘reat caution in renal insufceney ——== | Fibrates Fenofibrate: ‘ Goadad at abexpon hon ast 1 Seng dng opamp Lgl bl aus ur) ted mat eee {Theta sng mond helm ‘Shenton soso a ile acid binding seguestrants (resins) + lonexchange (exchange anions suchas chigideons for ‘feces ton absosble, Mockang the erterohepatc jet bese tal cholesterand LDL: holster by insbing the renbeonpeion of ble cin “heintesine + Unfortunate frequent occurrence of ie effects mits ‘he practical longterm admin sation ofthese dg 15.4.2015 PE... exétinib “nie a iearatterme ts, Samant Secs ceed neta tch, + Adverse effects: constipation most often, then nausea, vranee tcl sareriaetc, recta Maer Seed ee ae HERR + Drug Interactions: May decrease theabsorption off + Dis peropton i ot affected oo sausage soluble vitamins and many other drugs, so these dra ‘effect fot metabolised i 0. sk arsenite eee eae ‘encase eet * Agen opmnntea tet P| |-Nicotinic acid - Niacin ioe muti ypreiieboad cece erence Obesity pea eer errr «+ Accumulated excess body fat + ecie oaeypeno HP es tang te ne rier ‘ess outs gperday)aodted wi ADRS: aa ‘+ excesive fod-energy intake, lack of physical activity, eee and genetiesusceptibilty + sh cule ines yh dination fa allameunt + indused by endocrine disorders, psychiatric disorders servile + medication + pines rmoreing oon thn + Conant ens neh acnepepticlerdaese PE... ee ee BMI Classification Obesity treatment BML kg m= + 180, a0 Iolated systcic hypertension 214030 ee Prevention + maintsinnonnal body weigh eradueso body marindes sonskume) + rede itary sodtminihe og oftodumachlarde per dy + engage in epulerseobic pipe sty uch ae ke wllng (sominper day. mose dy othe wel) + linitlchalconrarptonea no mare than aie ayn en ‘noone ans it day in moe ‘+ consumeadiet chin Fritand vegetables(eg atleseFne porns pedo) «consumes et with reduced concen of sturted an tl Pharmacotherapy + ACE-inhibitors + Angiotensin Il ATa-receptorantagonists + Diuretics ‘Calcium channel blockers + Bera blockers + Alpha blockers and drugs with central mechanism of, action, eee, | = = ACE inhi Ors « Angiotensin-converting enzyme inhibitors reduce ‘the activity of the RAS. ‘kidneys release renin - acts as an enzyme and cuts off 10. amino acids of angiotensinogen (a protein ‘produced inthe liver) * These 10 residues are known as angiotensin 1 ‘Angiotensin converting enzyme (ACE) then removes 4 further bo residues ~ conversion of angiotensin | {nto angiotensin | 15.4.2015 /Renin-angiotensin-aldosterone system ACE inhibitors + bloc conversion of angiotensin Ito angiotensin I + Vasoconstriction, proinflammatory promotes hypertrophy of cardi myocytes “Therapeutic effects: + lower arteriolar resistance and increase venous ‘apacity; nerease cardiac eutput, cardiac index ‘+ lowerrenovascularresistance “+ Teasto inereased natriuresis (excretion of sodium in the usin) ACE inhibitors preferably used + eftventrcular hypertrophy ‘eheare file + condition after heart attack * conditions aftera stroke + ischemicheart disease *DM * diabetic nephropathy * hyperlipoproteinemia _ SS | ‘ACE inhibitors - adverse effects + penitent dy coh 1 hypotestanhyperaleni, aedace, que + Real ineton detrei - parca pater th ow Fea ls lo ern aay sno pov) whose {omerlrFleseanrae (CEN) tdependenon erent Sresearasocnamenonby anges renal arery stenosis * hyerenstiiy tO ACEnhibeors + pregancyané beaion |— Arigiotensin It receptor (atyreceptor antagonists or sartans) * Logartan, Telmisartan, Iybesartan, Valsartan, + block activation of angiotensin ILAT. receptors + vasodilation reduces seretion of vasopresin, and reduces production aldosterone * hypertension diabetic nephropathy and congestive art lune + well-tolerated i patients intolerant to ACE inhibitor therapy Srectrenin bor * Onetefacion: Maimun atypia ws $ Abomton Poo absogean decease! br high me! 1 Sota 1 Hae mats ag huang aur) 1 acm Urine set sted deere uncangdnrie fecS tomar eon sae + Eee neater utente COPS SAg 1 Afsngoedena bpetlonn Cl datrtees pesca * op neraae kol dere gace enone Cl Cageaanithan Einhorn aR 15.4.2015 SS ————| “Diuretics 4 Hydiochloothianide + Ghlothalidane 1 Indapamidesatodiattory effets * Metipamide 1 An ptasi sparing det in combination ose eepd terreno in + Spent: eur drt [aS Se on {rel fare type, regamey ee FThiazide-tke diuretic + Chorale, indapamidecloparie, + Okara dries oa observed withinone rant ‘tayo or sbou ours + Weed does hares dines 1 Aauiinpenenvectet inmor gradu n onset end oreo ian + Theft on idee depends up carton no reral table Reg eianacraagnes apne + Preferably ured in hypertersien and chronichet ale in hs patets lated sac hypenetson ‘cu and ena inetieney a Thiazide and Thiazide-tike diureties~ ‘Complications + Hypssyemia + Hypesinidemia + Hyperuricemia © Hypercalcemia + Hypatalemia Hyponatremia = ae Calcium channel blockers + specifically inhibit the penetration of calcium into heart muscle cells, cardiac conduction system cells and vascular smooth muscle — decreased vascular resistance + Systemicvasodilatation * Increased renal blood flowand GF results in natriuresisand diuresis > inydropyridines ‘edie tem vcr essence adel pee + amlodipine * Manidinine + Bamiipine + Nicandinine + eniaipine + Nifedipine + Iacadipine + Nilvadiping + tfonidipine + Nimodipine lacidipine + Nitrendipine + Letcanidipine 10 el ‘ae Calcium channel blockers Phenylallylamine verapamil + selective for myocardium, reduce myocardial fnygen demand and reverse coronary vasospasm, nda often used to test angina pectoris Benzothiazepine- diltiazem + intermediate clase between pherylallylamine and dihydropyridines in selectivity for vascular calcium channels + causesa drop in blood pressure and slow heart rate 154.2015 pera ges * fongheite += Metaboliclly neutral - donot adserely aft the smetabolsmofcarbahydatesand ip + positively fect the kidneysanipesipheral flow team + donotafect heat ate + donot frequently ause orthostatic hypotension + donotindace sodiumand wate retention ‘donot cause brenchoconstiton “lead to regression of lf ventricular hypertrophy -— Dihydropyridine - side effects + Dizziness “Headache «+ Rednessin the face «+ uid buildup in he legs + Constipation * Gingival overgrowth Calcium channel blockers Indications-suitable for HT treatment in patients: * oldes, * with hyperipidemia, IGT; DM, MetSy +1HD + cerebral vasculardiseases EE Beta blockers ceptor stimulation increases heat ate and nutes contact, contributes to maintaining ‘Bdequote blood pressure, by pathological stuaton Canibus tothe development af hypertension Ma soups cated primary in the bronchi, CNS ane Jes: Their blockade may lead to "ADR broncheconstrction 1 By rceptorynadipooytes IADR: negative metabolic eects cr oe ae — Beta blockers - Indications: - Coenaryheat diseseangina pectoris sete myceda infin sn monday prevention ha atackaer crereming Artesia hypertension Tetparthythmas + Terapeticelfects of lockers: ‘eductinof myocar metabiedemands(edactonin het "ae and oar dees) seein event esoson eoprteteapd ancy eer 15.4.2015 | Béta blockers — re Cardioselectve espana Propranolol Nall and Soa ntiarythmis), Nonselectve with intrinsic sympathomimetic activity Pindolol, Bopindoil Extension antagonistic effecton adrenergic receptors alpha etpl Beast Atenolol Seopa (aor Cardioselective with intrinsic sympathomimeticactvity Aesbetoo, Calipaal Beraand Alpha blockers (vasodilatory fet) Carel, Labetol ~—-Céntraindlications of beta-blockers ~ bradycardia = hypotension, ~AV block heart failure - DM with frequent hypoglycemia ~ pregnancy (especialy inthe thi trimester) ~ caution to patients with asthma or COPD feta blockers - side effects + bradyaychnias + penpheral vasconttion (td eet snare) + fronchoconsrction + Hague allel choles ghee LDL Biased ee + epresion lxpdcrder, sexual sfuntion 1 rebaand + Bets blocker therapy should not he withdeawn abruptly betavadyall tapered ers week to avs faeijcari, schema vperension an EE Alpha blockers + dec dade of trneereeporin the all 1 Swedes wet hyperopia peli Phenolics cer on pete “intr hoa en Alphat-adrenergic blockers privosin, doxazosin,trasin ration 12 |_Seléctive alpha-2 agonists + feehack ead toa weakening peciphera sympathetic tty action im peripheral restance,derenced levels ofreninand noradrenalin methyldopa, guanfacine tlonidine tiles a3 andl (imidazoline) ecepos. + ADRs: sedation upto 50% of patents onl se nidarain cea subtype (his Ceepesiypek fen he mablaabionga 3 ‘dress in ate nose cea {ioor nba moxonidine, rilmenidine 15.4.2015 >>> | fargets ~ Antihypertensive ‘Treatment General Population 140180 mmHg Diabetics younger subjects «< 130/80 mmHg Nephropary (potlnura

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