| ~-MBBSHEEP.CON (Pa) DAMS - | PHARMACOLOGY xa To beMBBSHELP.cO@2 0, ° fi ey Ph. SL & 0 6x Getweal Pharroacalogy ee eo * Asorbed into Systemic chrculatlon e @ > distbution at ov: e ys 7 alt over body P-Kinettes e 3: Metabott letabotisen ee Apme e e 4 Exereted ee haw dons * exit @ © > Fate 4 dwg to body Body tact to doug 18 Pharmacokinetics ®e ABSORBTION @ | 1 Absorption. Drug crossing membrane @ e eye drops- Conjunctiva e © Oral — gastric membrane , Topfeat- Sti a Fi @ e rast of drug — passive aiggusion he cavriey molecules ; © along gradient for glucose, Aminggycasides, have THahspe ee But drugs doo't have. Transporters. ee . 5 FlckS Lau ss Denotes passin diffusion (PD) 6 Determines Rate | Speedy Po e PD Be Pe ac x ax) Rs Rate of . 6 C+ Cone” gradient (Magnitud e determine @ Surj kate) face e 6 Jn equilibtum, ac <0, P.0+ stop A's Area available for absorp e e a mnonbra Greater Surface areas Grealer ec Ts Ticeness Y ne ae @G ~ Guster T + faster Absorption Pe Permeability Cougficient D\ e . Geobether key drug is abiai 8 Hindicator jet iphophiticity A ®5 F arg) @7 Drugs 15> Fluvourocil Caotiéancer drugs) - analogs of edogrrous 40 Urad! - pyramidine in body > By Active Transport “ + Levodopa, {oonrns Catecholamines, a to 2 &- methyl dopa. trdogenoas Catecholaratoeg > Sites op Absowptfons:- > *e_ @ motecule should be Lsindissodated to Cross meobrane, the drug Weak acid in _, not alissocfate Acidic medium not diesodate Lp Weak acids —> stomach —> acta, Amy weakly aeidic drugs: absorbed 79 Stomach. I Bu tforamides Atcohol -7 & Stomach Gest LBu Barpdtarales UN gals = mefenami a. Sman Intestine Geore, absorbed) acid, Ibuprofen efile Basic. drug > Basoptilie > Mistomine Release a Weak Bases of duodenum, Most absorbed 19 Upper Port £9: UA. Morphine + Amphetomines, cause histomine Gelease A LA: Polymny xin & Cantibiotie) = VSomycin > absorbed by Facilitated Diffusion Cie by Special coring) 7 fot. ARARADRARARA AAA AR Am hhe S-d- Tubocuranne non depolariting skeletal wm relaxant 3 e Compesitive : e All deugs which ends in ~ Curiun) ” a? move = Abrercurrium Lass. Cisatracasium Drugs ends.“ Curonium’ doesn't release HiStoming bee they ove native . Tabular Reabsorption :- Urine - 0" _ acidic - so Drug et distodate, so drug romain , but tt excrete drug Atkatioat Aikalanization dene for Acidic drugs 7° Done by Sodium Bicarbonate fngusion = e@ e@ e@ e@ 6 e@ e e e a for asic dnugs for practical > Acidificatfon Ts ovelded. ta ctiofeat Uric acid, cysteine. get deposit In wring 40 form Stones 3° Bioavattabilit + How much of drug 1 absorbed- - % | drug administer that enters Sypfemfe circulation in Uncha Four « 7% Determine Rats axtent gf absorption 7 Mest: imp: factor that detemines gi Availabilty Is ef Route of administration = Max- Bisavaitability 5 Inhavenous loo. ‘ Entire drug amount injected into Systemic Grealation e ° |aghe giing drug to 4 won single dose , we plot cone? & Time. é Avea, under we gunve 4 v . Time =? give. Bleavaitabttity é « 2 Oral Bioauailability:. é 1 Incomplete & o absorptfon é 2. Apher gelling absorged , before getting fot systemic Circulation é - q Ge pass inst - pats metabol’sm- é Factors ef deug:- that decrease absorpKon:. Orally: vt Polax compound jonised oF dissociate ‘ Egy @ Aminoglycosider * shepto & gentomycin. ¢ Administer paventeally. because net absorbed orally. ¢ Be Neostiguine - Quaternary ammonium compound act Crocs aiotegita © membrane - € ~akoays given 1M. € 4 Physostigmine — 3 ammonium Pass membrane - é labile —, orally Cleaved #0 Stomach itself. So ¢ jv € C it win chave in gate 2c1.C a. % dug is Acidic Pencittin G (@enayl peneilin) — only 2. Erythromycin (ovat) enteric Coated oo" a ret enteric, 3: Proton pump inhibitors - enteric Coated ¢= COCHHCHOHHOHHOHOCHO HCO OCOOCHOOCOOCO OOO OE ce POP SGCOOOeLOAEEED DE DD 3 Eraymatic Cleavage in @its Trsulin et io GIT drug is protein , it fs cleawed to re dug is Prot ee. €g- Insulin - which is pepiide- Q se Onytocin, Asparagicase, vasopressin, Desmoprestta , Somatostatin . 4° Omg interaction 1 Ak abaorptfon. 2 At Receptor site 3: Plasma binding. ete. fg b Antacds — J absorption Any diug + Antacid — J absorption 2+ Tetvacyetio. absorption L by Catfons. mK Pca + Tebracyclin > Insoluble, complex eahich iS not absorbed cation (nor given with chelation Ton att ink) t bw 4 absorption. Interaction % Food: It not only * but ato ae J Absorpfion 1 Ampieitin a Aspirin 3: Captopril 4» Digoxin 5+ Isoniazid CH) ° Jan: Stationery 6: Levodopa 7 Rigampicn (@)) Gautam NAGAR 3 Tetvocyetines X tmitk, Food , catfons, O9bsYyeai1: Conbamazepine 2. Chloroquing 3. Gpiseogulute (Fatty Food 4 absorption) 4. Lithiun @5. Lumefantrine - Antimalaria - Avtesunate + Lumefantring 6+ Nitrofurantoiy - Urinary antiseptic - R, UTT F + Riboglavin- — Symthetic form ay Vt By 8- Spivatotactone 4. Exlotinih — anticancer dwug. isro:- PM. Me'- Liver 1) Oral ——» Liver Admicisteatin (FPO) Active Transport PLP ~ Coanayme @ D-decartorylase. Wee L- Copa + Pyridoxine 9 PUGS Lith high PIM nob given Orally = ovaecashand Pee in Ko Tipati Hadrocorbton Spates) Isoprenatine Sepreneiin J oral Bioovastabitity Lignocaine Testasterone DR & & & BM GQ h Th Dm Bw a ON RN NO2: Disbibation:- Drug's given orally io high doses: , with high FP - 1 Peoprona lo) Yop tects 2: Alprenoio! 3 Salbutamo! — B agonist 4 TG } evs drags S- Verapamil 6. morphine pe § 1D opits T+ Pethidine @- Methy! Testosterone 9. Propoxy pene Distribution F Volume 9 distibution (vy): Vz Dose administered a we Tromediats plasma cone? wore sco + Mg 4 dug tow =f plasma cone” dag deposited 10 F plazma (because in plasma, Pret tahich bind) 2 Intravascular Gompariment SOP COROCCOCOCOOOOEDED0008 2% Md * ~ | plasma Cone” 1 vmg gow foto Hssues w deposited eee eee 7 Va gts about extent gq Hscue penetration eo oy ft vg f Tissue peoctration Tain Station’ @ @> va pray einaung - 4 metabousm — delayed — * (Ppa delayed excretion € Drag become long acting . ‘ é 3% PF PPB igh incidiner ef drug interactions (unbinding ons beads Toxiiy) : . « o> Wt — 4% Tissue penetration ; ~ tg Chhoroquine - 1000- I200L - daposited in organs « J be Meuinly in Lives € ® for amoctie. abcess 3. geting. — Retinopathy é cause Chloroquine Not five fA other € ™ ue \ exats exe Macula 5 amoebiasis € (Chiowguine Retinopathy ) => Chloroquine: é Tt will leave Plasma y enter into Hssuc é € ~ $2 Woacting dose y chiowoquine given because. 4 Nigh @ 4 Y Plasma concentrat”. @ @ Hemodialysis :- factors List Metabolism F Iow Vg - tow to moderat, PPB 2+ Tricity drug (more Toxicity ) J drugs eliminated by Hasmodialy sis. } Corbamazeping overdose 2 overdose (i 4 meyh) 3: €ythelene BY Cor potsning — move excupatona Heserd. > Anfifrees in industries 5 metylalcohal Poisoning methylene -e /@ x) ee ee ee ee eo eo i | ©°eseeenenans © FF 3 S% 6. Phenobaxbitone 6 F Solicyctates overdose | poisoning. > Theophylline - & Valproate. - Metabo tien 1 Fore whieh Me ts fo Inactive become active fo Body . Predrag Inactive Active ( ody) ™eabolil: Ionelive — Prodvug egubneyetouty 5 Acycloutr triphosphati (Po, 3, Phosphorylation Stimes coq 2 Valacyciouy 7 acyclovir —_eppovit (Poy, Toa ctive - Foe 3 ACE T ave prodrugs exapt Captopril ive Form Listnopstt Analapyit ———> Analapril at yn Enola prit > Enalap/at IY fa Spe 4. Cyclophosph amicte Conticancas ng) > I Aidophosphamide : Rutherapeti y Toncty < 9. Acwlene—y Resposigne HA temorhage YStits 3+ Phosphoramids mustard. 4 Respensitie. A Therapeutic ‘feckDrug metabolism :- Coup, wove lingth at which ‘45> max: light absorption Cytochrome Py sy O- Phase I veactons & Phase F Reackons Coppositi, Reactions) Oxidation Rest all. 1 Acetylation -> Acaty mocity addugl 2 Reduction 4 methylation» mettyi! mocity added 3: Decyctization 3: Sulpation > sulphur- added 4 Cyclization i Conjugation 5+ Hydvolysis I. Glutathione, 2 Glucsvonic acid ~> Glucorintatie 3 GYycine Gilitubin Endogenous metabolised by Glucuronte acid Uke 0 xenobiotes Deugs undargo Acetylation :- S - sulfonamides + Di & Structurally to sutfooamide Diamine ot H ~ Hydvalazine (Pfamine of Pheny! Suiphod I ~ Isoniazid P ~ Procainamide’ Pp. Poroamine salieyclic aad (Pas) C- Clonazepam > SLE- ita syndrome coused by S Lupus - Whe Rath. i drugs undergo P eeatylation . & é ‘ é € € q « « 4 q « é é « 4 q 4 q € é é é ¢ é ¢ é2 CYP enzymes e ae . ie b All CYP enzymes undargo Xenobiotic veactfons. - . . f - Rest alt e 1 CYP 3a, most q dnigs are metotolised by Y's (me)- Rest al e - Predominant enayme e 2. cyp 206 @ 3- cyP2ce/q @ e Y cypacid e SS cyp 26 + Drugs metobolited by CYP 206 a ERE : @ | Newoupties (Typical antipsychotfes) e@ 2+ TCAs Cantidepressives) e 3. ssezs, of ee GA Aotiawthytimies. oe B- Retatiocters 4 caweditol ee © - Codsing 5 morshine es Gn Cotedy) @ @ 6 > cyP aca/y:- @ @ I+ Phenytota e 5 e 2 Warfarin eg eg CYP acla:- 6 ; | PPLE Lite om ° $ Lee ome. omeprazol eo 2 Clopidogre! Cantiptatetet ) eee oe 3. Voviconazole Geokifuagayyuv . couse GI Side fects gestits / 5 por b Clopidogrel is Prodvug . . & Tobibit clopidogrel we give. PPIs & Clopidogrel given , PPTS to mS Omeprazel (mast) hich Is prodrug S0 better Pantop (least) give. -H, blockers CYP Enzyme Inducers 1 CP Emryme TOMES R * paduer do 439° 4. Exytinomyein cause toil 1 Rigampteto fompi Precipitale Therapede 9. Clarithromyto es . lever vit K Can't 2+ Griseosuluta + keta conorote, Cause Emyme. 3+ Carbamazipine aa) ; Inkibition - An ant epflepte drugs except Valprote 4 Isoniazid» Phenytoin Phenobexbitone F- Alcohol + cyP2€4 hn GPRS Cc Phone » => CNP REL: 2. 3 4 S- Oflt¥aam acid 6. verapamil F * Cimetacting 8 Ranitidine - . 4 Valproate 10. Protease Inhibitors Grape fruft Twice except ft faduce CYP 264 Conversion @ Paracetmol to NABQL-: NAGAI T > Hepototorcity Alcohol TSoniaxid j T tem Toxicity 5 T NABQI Ug 12+ Tsonioatel > anbjbits all CYPen2ymes XX AR OR Md A RY BX GY MX BR MR A BR wD « é & & C Cc-\|s | Exexetion 3 ee ae @ e © 4 organ vesponsiote fa txerttion:- Kidney e Sctturedion kinetics (saturation e ee elimtnating @ © onder Kineton Zero Order Kinetics ™ehanién eé © @ | Lnitant fraction is _ Constant amount % drug is @ @ eliminated in unit time eliminated e e - tone oa 200%g/ Ut e aj Pama, - tomy ent @ 2emg x in I-min ee to Fm — sory —_ ee oy. of Yoo | Rorng .f min. 400 eng f mi ee wer 4y ee eke @ Rate of limination Conttad- ¥ ] Rati a elimination o plasina cone? q e e, (Roe) Indapendent Y Plasma cone? e °E = Dose Cx) © ws e@ @ ©? Th & Clarence constant Tht, wd z Pio dese. cou ee + with f plasma cone, ine by T ee to dose the Ty, 1, Clearonce ee carne e e Alcohol > 2¢ wilt fotow at at dor e Ta Phenytoto e® ae high e pa 3. Theophyitine oral ° e thee $85) 4. Tolbutamide (anti dfavette , 1%; e eos] Suyponylurea to 6 tn bow) WwW - 5. warfarin @ 3° Soo 6 Cetuximab (Monoeione 2 © : So thee amticancat. °e fey ets F- Satiegelates may A may— | The Require fo plasma conc” becomer Yo - measured. to units x Time. Ty,+ 0-693 k Elimination vate Constant: Ty 2 0:693 x Va Ye cu é € Ty, drug %% Shovt 5 Plasma cone becomes yo Fast, it is ; jetting excreted getting € Ty, short > Raptd elimination from 2 Body. > short duration Gacfiogys: enly Some amoent Timate long -» Slow elimination ‘fon Body. tong acting € * @ Ty, determines Ratt g elimination g a drug 4 S07. € Tn 1 TY, how much q drug diminated ITY, - 507. aT + 757 3 Ty, + 04-57 PD he 4 TY. > 73-257, 5Ty, - Vas Never each 1007. A drug is neuer Compete eliminated:= level y Signiptcance > 95, then considn 7, ~|~ Almost comput, elimination ee almost equal to loo, ine ST Hy, ee . ee : | Almost complete elimination occur in OT (4-51) eo ®& © &xsq, , eorance :. Tells Abit body to exexete drug. eo 6 () 3 4 3 ee J SH Wo CL , drug accumulated ' plasma Cbodyy Se e Pharrmaco binetica:- @ BSS nits e - : 1 . " ef * Bicauoitability :- Rate u extent Y absorption — no ,thath, © ® » Vd © Tissue penetration Lit per tg got ee . 3. : ee Tye © Rate gy elfminaton ete ee &6 4 CL Abitty 9 body 10 excrete drug, Vrinc? Peto @ of 3 state 7 7e Steady Cnuntration & Plasma CcPss) @ © 7 Plata cone? is fluctafng and at one polat it becomes Shaipht Une, Successive TY, Lins > dnug elimina The oa Ya- ahys, — plase loo: ng lit * abs | aTh) Plating Conc? become. ‘Soma aha Constant | 45 eliminated 35 CPss acheived STy (4-5 TH)(Lo . x. ow . F (efoavaiiabitity) : . gr Chloroquine» high Va > highL> Lo = ug Target plasma cond €@ « @ 3 Maintanence dose = CPSS% CL e Coop F (oh Bioovaiiativiy ug sua tly — @ * the F241) e MD depends upon CL = Urine con? ‘© ovine Floating ee Fie Ye mys Clearance Playa and @ 2 Dosing gy drug depends on Ty. ~ ¢@ Ke Monitortn: ° Teeapeattc, Prag Hooilng «es (Tom) i € . e@ > Plasma (A) Blood wuels Y drug. @ 6 é ‘Indfcations:- e €@ 1. Nawous Thereupetic Index. y drug. no a High toter individual varfattonia plasma levels ¢ @ e 5: oe apect J drug canlt determine Undividually) CUnicary € 5 € 4- O guing epheotexic drug €0 Renal Failure patient - a @ @ 5: To moniter pt- Compliants Cpt- tating drug & not) P 9 tg &£ @ 6. Detection y Poisoning - € je g @ Dugs ich wake Rae < @ a ° Hove Ce ae wo 6M > Methotrexate on A- Antiarchytheies antes Noo? weed catetnesate, tkevtors ¢ gre?" T — Theophynine pre Calcineuvin tohibitors Uke . e teat Le Lithium cigctospovin C @ A Pecinegty coSidey Tecrolimus ° A antiepilepticg D> 7 T Tea Z € @ @ @ @@COCOS9HOHOHOCHOHALBHOEE EO ee Peeeceeeeeeoenoonleg Phormaco Dynamics 4 Potency:- The dose at which Response begins . Drug stavt vesponse we at lower dose ts more potent Therapustic. measure Should be Same 10g dose —> Csame group) tog dose Response Carve Core) Sigmoid a: Efficacy:- ‘Shape > Maximum Response altained by Are amg Bp> Ap > Doex da not depend on Dose > Some therapeutic measure lag dose > > Io clinical Sceneria, Chota Y drug is Efficacy. —' > Doc depends on Efficacy. Zo Dyslipidemia, Hypertip'aum'a . Goss to fats LOL Cholesterol . » Fibrate 2») Chotestyramines 2) Btertins —> Doc .-p because high efficacy OF Efficacy 9 2 drugs 1S Same; then poles Safety re lesser Side epee iS consicuned ass Sac gre: Nocturnal eneurisis » Desmopressin 7 er rey & TwipramineSoyety:- determined by Quantuny BRC 4 a Populafon roagetiode Shrusing of apse “response tog dose > Weg dase > Quantal ORC Fol Therapeutic ng ove. ak 2 Toxicty 5p thraunt. doe tn ap Pepilaton, tant of Dag PY TOsp Torte dose to Yn of Population , Ts on Indicator g Drug Safely co LOso (Lethal Dose) EDs. L0s0 A amg 2s pore a seth looms toomg Ca a a a a a a a a a @eeeeeeeeoeeeooneeeooneoge e008 0000 0 Ot 7 X - Som & €Dgq - Img 4smg. & COso € f LO, ¢ Therapeutic 2 50 ingrcater fet Safety ¢ Index Ed.T | op Therapeatic: toca 127 Nt ee. pr = Safe ee . ® 6 <2 ‘unsafe re Mavrow T-2 ° e ° Recep oe ©& eceptors eo é GABA Receptor ts classical eg. gy 09 channel , open fa CF ee ee Ligaod aed, ® e ° {ocean @ eS } ~ Proteios (to reesult appropriate, 24 messenger) e@ ef& 24 messengers 1. CAMP , ee 2.0 GmP ee 3. TP, [0G ee Adanyly! Saurgtt . . °° ny A LUIGS wach donot. Nite. Oxide ° ee NS 4) Nitrates e L Reeptot, e e c Amp cae or uae by CL e Jremmuae by © a ee 5! Amp Diesterase 5 ~ GnP (Poe) ee VOD mettyixanthine ee | Sildinagthe e@ a a thee fT CAMP, Pegmp uy No donors,” PDE tohibitors e e there uth be Staletat/cardfac— Contraction Smocth ms — Relaxation ( Btood vessels) Cause Vase dilation. al PS 8SI+ physical Antagonism: Astagonism 1S because qy Some physical Property tr mass , charge, adsorphion etc. 4 Activated Charcoal > reduce oral adsorption, 2. Chemical Astagonfim:. Chemica! Reaction, «gx Chelating agente to In physical & Chemical antagonism, Direct binding iw 2 drugs 3: Physiologie » 2. Ba 4 Pharenacologie a Heavy el pofsening Csatg hydra groups) Recaptore are net tovewed or molecules A is by blading differnt &S antagonism: of antagonism Adrenaline & Ach fo Bronchial Smooth muscle u Histamine. te 6. constriction Ingulin & Glucagon vo 5 Seid gucose aid glucose Thromboxane & Prostacyclins 4 Vaso Constict” — VaSockilat” Antagenim:. Antagonism — by ach & Atwpine at Sromchal smodth eouscle + ¥ Constict® dilation act 00 © musturanie, C's Adveraline & Propanalol =o SR BR MR AR AR OR Nm a, Om IX NmS9@CCHOKHCOHKOCAORADO OOO FPPE REDS oe ee Pharmacological Antagonism :- @ same. WW Gioding Sits Same $0 competition dunlop % Agonist & Aatagonict binding Same Receptor Competition occur - 7 5 ftive axe. Revers Competitive Antagonism of] Most: competitive % Agonist & Antagonist same Recaptrr but different binding Site ie Allosteric Sit Noncompetitive Antagonism. ToSurmountable ax ogy] - most NOnCompetifive OM Reversible. - Surmounta tte Antagonism: 94 competitive Antagénisn fs reversed 4 agonist uit displace antagenist Reversibie :- Antagonism:. 8*5¢-kioekes Antagonist bind 10 Receptor g Ht digsocfate Spootancous Irreversible, Antagonism: No Spontaneous ssoefation. PW Noocomperitive Reversible €9:- Carbonic Anhydrase Inhibitore €9> Brenzolamide TAIN STATIOVERY GAUTAN VAGAR © 9654691 BATE © FEN F82444 q“h Recaptors present foseNucleus:- - oh i £9 b Thyroxine an gooadal steroids 2. vit A. > Estrogen 44+ Testosterone & Progestesone 2. Cytoplasmic Receptors eg & An stewidat R's except estrogen vitD B- Call Surgace Recaptors + Rest all- Seulin, GH, Opioid CUnical Tefal s 2 4 mandatory phases: 1. phage T 9 © Small a phase F yasmalt group qj Pateols group Daly volunteers 3 Phase fi —> 1 sample size 4: Phase W -> Post voor kating Suxvelldance (PMS) martsing drug). => Parometers:- u oneus: to > Efficacy better studied Bat to fi Phase but action ts nucleors, Receptor Family . , torge group of Patents present in nucleus ts Innucleas SO Family not 00 (ab animals = multiantte Study = congirmative Csurvellance, ager Tit Fe to patients BY BX ON EX ER ER FR AR BR AR A AR A KM AAA naevi~ eet Safety - Studied te both healthy & fn patients. ee - stidid in phases - 2,0,0 ; e - Gest- fi cS 6 @ @ 30 phate Ts Evaluate Safely, Pharmacokinetcr, Pharmacodynamic: e ot e © - Phase W :- _ long term side Effects (s/e) ee c ee - Rave sfe @ e - Efgect of drug on Special Populations i pregnant uw e ’ . 7 x e . . lactating women , Liver & renal Failuxe Persons. e@ - Tt 18 Reportive phase: . ef @ © = Prrase TF Effectiveness veseareh eo Vig uncontrolled Condition i-< Community. e e Dugs Studied in Gntrolled condition —» Efficacy, @ 6 ‘ E ee ce Tk ts active surelitante effeckveness and tt ie oot Se Sepovati Phase but Te 18 a pact Y phase W Preclinical study: SSS Tt is careed out on Lab arimals , before Meoratfeal | Phote O: 2t fs Same a part ay Clinical Study - mt is micro Dosing = @ Smal group healthy Patients given Sub therapeutic: chose, ~ Evaluate — Pharmawkinetcs —> Gioavailabity > Performed bjs Pha I & Preclinical PPS Soe eos oGood clinical Practica GP = + Clinical Tefal under Some guidelines > GeP studies not used Good Laboratory Pract ‘ A fab Himes > Some guidaios worelog at b > + Requied to prectinteat, 712 > wot required to Phase WW 1 Salix alba —>&, Fever Salieyolate 2. Bore. a Cnchona L Product —— malar’. Quioine Catkatetd) fo Preclinfea! study - Th DR RR A NAN A AR ER BR BR ER AM RM @SGeeevneeoeoaegenegaeoeseoneognneongneanngageooeveodes Om@o4 eee eee SCECOOOOCLOR9REBHRO0O008 Strucheros Drug Des! tgoingl sop Computir Assisted Ouig Desigatag _ CAoD $007 Crug duafgoed bY Structure | Tdantigication Crash Recaptoy- > Enayme + Hma co reductase > Signal» K-RAS —> & malignanay Protefo . Transduct Gat proliferation &- Determine structure gy Target 1 X-tay erystallography , Avamospechography jecule ve Ugand - > designing a New mol to target a This ts known ag Target. bosed Orug disigning Detigning by Structure based on Structure Y Target ee existing Structural modiigicatons q aPreacnt Ligands - Potential Ugand - bind to unwanted Target proteins - a Lt good based Ovug designing | 4: Non Towet Proteins : Ugand ea it causes higher incidence ¥ S/E Ligand > Torget . Protein «. To L sie July Non Taget 1D Specigrity to Target Proteins, Protans 2 Reduce toteraction Enon Targe€ 1. Drugs for treating ave disease: os 2. Commercially ot Valuable Viable - é 3 manuactuxe ancouraged by Govt > Fox dastysing & development | g deugs. € é N System ‘ ti IS: Autonomic exvous ; Paxasympathetic, Nervous Systen'- 4 é My Reaptor : Location tn Gq 4- cns| — Ach excitatory q : Neurcotransmitted é © é O——Kacheg_—___< 7 : € Cholinergic Transmission in ems is via My Receptors é Tnvolved 19 1. Leasnteg & Memory € 2. motos. pathways é € => Dugs acting 09 Mk “ ing K Memory := D Pearaieg “\. Alzheimer’s Oementia- Degeneration @ Cholinergic, neurans Y cholinergic Fransmission € A Transmission by Centval_ anti choline Esterases C es ¢ | Taerine Oy FA mild tomedetale, Rastiosonk diag Rvastagning 3: Donepeail —tong Th ~ Tohes ( 4+ Galantamine . @SOCOSCOCHOHOHTHHOOCHCOCHHTTH9HHTHHHHHROHHHHHHOtClinicfang don't Use Tacxine because it S/E hepatotoxicity Ib vi~ ele @le «_ . 2 F f io i - NMDA ontagoni: + Memanting used in Ab 1s disease 6 @ antagonist «§ = a) @ => Motor Partuoouy :- Extra - pyramidal Cnigrostatat Tracts) @ e fevoluntas y . @ @ (wot ( ee Ps > Ach excitatory neotransmittor > My 7 e e > Dopamine 0, ®@ fobibitocy necwtransmitter ee Ba, uf ° le “el eo ® Oo my ee ee Parkinson$ Disease: ‘S Cholinergic output is seen e@ . e QT Dopamine | Y ACh e ® Loo, central Aoficholinegics - L-Oopa ae ~ Com rotors * Titbexy phentdion.e e 6 - Amantadine Benzhexol % doe tn = Promettaat toda °? etbazing 8 | = e ‘ @ fo this D, Recipog PU ON ee . Bock, ee? Gastric glove 2 4 gastric acid Secretion e@ Ketone’, ° ® M, blockers :- ® Histamin, by €c culs e & 40 Peptic ulcer Disease e 7 . @ Plrenzapine & Telenraping (M4 Selective blockers)I. Heowt - we VER ss ; ~ V conduction ; 4 He- Chronotropics —vt effect by M2 « « J conduction - Droroobrapic —ve effet bY M2. My agonists: ; SIE = 1 Bradycardia € Yue ‘ 2. AV Block < 1 Conductor ‘ @ amet 8 cardsjo, All Chotinomimetica U Parotyrpathomitnencs eause trady i & AV Block. é : . € mM, Blockers :- Aoitcholioergic —> = Atwopine ‘ used Fol Av Block € SIE * Tachycardia - ‘ but uselaReg av Block. ‘ Ms Receptors: Location :- ‘ é we Activate. My—>l Smooth muscle —> Contraction é é te tris Cause, © ytract foo wm eyes Sphincter pupiag to Comte con’ ie 4 : Cfreulax muscle Y miosis ss . miosis . « “My Mine Ero nucleus —9 CiUary gangton

mioti ofa, 2 Trak ° e Trabeculax outflow used in Glaucomdb 1 > AntichoUnerat ‘| @ =PAntichitiogics Cause mydviattes e - @ 1 Atwopine -» int fatic i e Atropfoe_ pint. fe mydwatic a Choice to children , longut od @ e 2+ Hormatopine ‘Adavatieo @ °° 3+ Cyclopentolate ie 4 > Tropicamatde - ee? Indication a Oydvioties @ © ° e Ang — opthalmn examination fot dilat? of pupil e @ Atropine roping = Ry fq Ant: Wueitis C tridoeyeliti: oe idocyctitis) ee (if pull o frig away from ate © Past Swnechion “4 cae ° s Prevent formation Past: Synecht e © “Cholromineica used 70 Glaucoma - @ > Doe Ant- uveitis 18 Topical Stews which have. e 1 Ao inplamroa! Se tory Tole oe > Antichdlinergics Contraindicate in gaucoma because ft furthers eo Reduce aqusout out flow &¢ — Anticholiners i yess Clopleg pics are not only ™ 5 but also fa G6 ¢ é m * am ° paralysis q Ciliary muscle) - 6 e ee ef% Me block, bronehodilation Aolfcholinergees act ot Gronchodiators Ankichottnergtc. €g Ipratropium Brmide Gronchodilators:- Thiotropium Bonide . Oxy twptum Bromide Indications.: |. @rondhal Asthma. 2. Cord (3) Viscexo\ Smooth muscles - mM, —> contraction motility Io GIT) CParasympathetic) Mg agonist» cause otlty Uses 1) Post- op atony. (post opesative Pavaly’ “ Chotinomimeticr ave “ted - > Aniicholinex gic. drugs eC) Anti spasmodic > Dfcydlomine (a> Hyoscine Buty! Bromide COuscapan) W Ueinory Bladder: — Outrusor muscle» Ma Mg activate Celrusey will Contract Above urine aS Poratymp — Urinary voidence Internal Orethyal Sphincter %, fubtype jnvolun’ : Recap A S¥rmPathomientica cap Aoticbetina gic + Coute Contraction —> Retention Urn ie Hens) ‘relax mutdeg. used for & € é « é « é 4 @ é é é € € € € € € € SSCOCHSHOSHSHRHASHOSHHOHDOFGOHSPDPHH9SO9RHHH9HVROOE ¢ G c C C G©0800 00HT8OHHHTOHAHHHH HOt SCOCCORCOHEAEDEAOQALE ®6 Mg dlockers velax —> Urine retention of, agonist contract —> Urine xetention Ms agonist of, Blocker —> Utne Voidenc, Cholino mimetica 4 symphatolytica —> Uoiding on me nines | ArkiCholinomime tice Y Symphibel 5, Retention g vein (In opetd por theter*sation 1S 79 Organophosphorous poisoning Usraxy “aie - Atwpine Used 248 must to prevent getentfon ay Urine due 10 onticholinergie Sea aoe al few ; ° nth Cholinomimetics (Bethenicor) > Post operative urinary retinton &, ’ 4s Pecapion Aganist - Selective Aotichotoergies 28, Unstable Bladde, Ry: Agonist Ms Glocker Lankicholiongic Rt Oxy butinfn -0 > &, agonist not used due to se 2: Tolterodine 3 -Trosptum. Non Selective antichdlinergica ’ Selective Ma, Antichotinergic, :-4.Oaxf fenactn much efficacy, S Solepenacin > ¢. Flovoxate J etbtnonal anki cholinergic uted fo ¥* Imipraming unstabe Sasi | |Cant cholinexgics Ry * 1 Preaaneattitte. medications Glycopyrrolate” is an anticholinegia used a4 PreaneitheHe medication. Nicotine Receptors Nyy Receptors = ' N= M Juneton:- Cause ‘ Ls Skeletal muscle contractfons Ach contract both Staletal via Nm Smooth viat M, Ny agonist - Skilatal @goniym. contraction * Skeletal |- Ba | Myfithenta gravis - weakness a thotincegic £§* Nesoatignine _Anticholinesterase Prrridostignire. 2. Cobra bite Neurotonic Resp. paralysis? death Neostgnine Post-op 3: Reversal of Protongad Neuromuscular blockade !: Neostigmfoe. (Surmountable antagonisro Competitive) XR RN BR PRR RRR RRR RRR Mm oe @SOCHCSCCHHHOSHSCHHHHHHHH8TH8HH9HRHHHHHHO'NM Receptor Blockers: Relaxation oy Skeletal muscle - Q, rlused as Skeletal m- Relaxants ~ aused as adjuvants tD General Anesthesia. Dowcutonium , cfeatracurtam, Atracurium , d-Tubocurpnium, Pa pacuronium . © Autonomic gongta — > Pregangtionic qy both Sympathetic & Paxacyep . Capa gage Aehapt Receptors cause Transmission. @HGOO9HRHHOOKBOOd 2208820800001 @ © 4, harenal medulla 3 Catecholamine release by Ny Receptors. ee F > modified Sympatoete ganglia, ee e , s Ow cus 5 — cause excitation / zobfeiton depend 0 location.Todirect Divect Ce By * levels y Ach by Divect act on Receptor . & ; AchE © J+ Pilocaxpine = miotie , non selective Acetyl cholinesterates 2+ Bethanecohol- Ms selective , Pest -op vénary ‘retention 3+ methacholine .- wonseiedive = Indications petite. 1) Atropine patsontng < Mc: cause © Tatrogente pone seme i ills tcnexaie alkaloids Uke Hyoscine , Hyoscamine 2. Dhatura poisoning — ‘Antichotinexgt Ot" BD's - Oryness: 3. Atzhefmevs Ofsease. (indirect) 4. Glaucoma 5° Dost operative atony. 6. Myasthenia Gravis - Neostigmine - F Cobrabite — Neostigmine © Reversat a Protonged post “op VM blockads. a a a a a a a a ae DO m aoa R4 Ve ee Antichotioergtis eo. ° e Indications:- @ © biti \ sonic Ach € iokbition e OP Pofsoni 04 sc Doe - e > tedivect + e ® Coxbemat. poisoning Atropine e . .f, . a ee 2: Mushtoom — Amanita muscurana - MuSCasinic— Direct acting Cholinomiay available as : © 3. Motion stekness —G(seopalamine> Hyoseine (Fransdamal patch) 6 Poticholinegic. e e e i 4. Drug toduced Parkinson's Disease i o® : @ © © Peptic vleex disease a t- Pirenaapine . @@ & AV alock: a Atropine ee ee AS mydriatrica -- Cyclopentamine, Atropine, Homatropine @ a e AS Bronchodilator 70 Bronchial Asthma & CoPo @ be Antispasmodic Anticholinergic « ef 4. Oostable bladder. e6e ee Preanesthetic drug. SO skeletal muscle relaxants - d-tuboCureniim ete « ee @ e e o® TAIw STATIONERY ee GAUIPAM VAGAR O96 S4CHU3AF Oe 0 98 llag2nyy ee °e @Botulinum Toxin BoTox -Coiacks Presynaptic n- endings) BoTox :- Uses! 1 Cosmetic purpose 2 masking @ wrinkles 3. Aotispasmoai action by 4 Ach vekase In Achalasia cardia. by using endoscopy aiving SO7OX inj LES: CLows eCophageal sphincter) * uy. Spasmodic. olysphonia. S- UMN lesions — ANLS ; PSuuclobalbar palsy 6+ Chronic muscle palo J» Blepharospasm. 8 Strablemus Csqutat) Sympathetic, NS Endogenous Catecholamines *- BRAM OA A ® O& M&M MR HB E&OE ED RW 4 1 aympatiere Hh tired

acts 09 all tt uslll act + Nor Adrenaline ve —7 Not act on (#3) , 09 Rest Dopamine. > Dy > Dy Receptors. C0, 1 Os. Ps by) € ¢ t ton LKB, Enogeoous Dopamine {fo high doses ac’ ri < . Keceplors ayp Adrenaline :- uses:- bs Anaphylactie Shock. — .00¢ - Z/m Advenaline o-5mt gy tle oo: 2. One drug to Cardin Pulreonay Cerebral Resuscitation CcPR W c ‘Pek! 3: Et ts used as Adjunyont = LeAnesticr CLigoocafne) . %, Reaptors :; Locatfon 4: Smooth muscle —> fentraction Reeth maset Mg cause Contract? - miosis — Sphincter pupiliag @ cause Contraction - mydvasis - pilator puptilne a Sympathomimetes cause mydviaséa:- 69 Phenylepheing prefened in elders. b Ciliary m doo't have . % Recaplors, devia qceplegia Cocafne— couse Cycloplegia Zout mydriasis. Phenglepinine — can't cause cyeloplegia 2 mydwiasis Antichotinergics- Couse Cyeloplegia & myiasis - D+ Uvioary sphincter — 4, —» Urinary m: Contraction ->-welertin Birra \ Orne CRuke voiding of urine BPH —s1 Tamsutosin 1%, 8 Selective blocker 2+ Urinary voiding ® cause Svemptomatic. tmprovement Sony For symptomatte: RellLv = Dutastertd, 2 8 cause vecluct? in Star qy prostate. dus to 4 prduetion 4 €@ (Shfokage 4 Prostate) ¢@ Dihydtoondtostevone Cuohith 1S andsogente SAmulus) e « e 3: Blood vessel :- Ce %, Receptor —» vatoconsitctr —9 TSP fe fe % agonist used 9 Shock ce Somatostatin, octreotide cause beltes to DBP causevaro g @ Const & Blockers — Antibypertensives > V8P- € e « e - Agonist fi A= Blocker. Cvasodijators) = Agonist Cuasoconstletion) €@ 1+ Phenyl proponalamine. (sot used fo shack) a ce Ce = Cron selective beck ait Subp, @ because gfe Hemorchagic Stoke . 4 Receptors) . — ” € fa Phtochramecytoma became. 2: Xylometazoline i 0 5 ‘ ; ¢ @ Predominant act" % long duration y action F e 3: oxymetazotin in naka! mucosa K- blocking. q e 4 Nafazoline Wid Flow dito fe L vasoennstilan 2 Phentolamine € @ Wied of Nasal decongestant O. nonselective X Blocks & @ Fade wame:, Nasivfon / eal eee) © |e OTTRivin eee « @ €- Clonidine withdrawal @ Long term Sje:- Rhinitis medizanentosa, because tt ts Short acting, € e anug C e 3-Tolazoline: ¢ e non selective af Blocker. e Bir Vato ditatoy fot Coronary O: e - Spasm. a aS g e@ @ ®Glockes wn 34. Prozasin:- , selective Block — Votoditator =Ry fo HIN to conditions a Scorpfor Sing. Prazosin eat Podling a blood io peviphey s« cause postural hypotension. * dose epect is am 1 Prazosin. Classicaty. 2. ACE Inhibitors 7 Start low dote at Ged Time 0-5 — Img OD HS Lv 14mg ao res 5: Yohimbine:. o€, Receptor Sek blockes = No Indfeation to use ~ aphrodisiac 2. CNS ie Egil Methyl phenidale - « agonist = Amphetamine devvatéve SIE Euphoria {abuse reactions nat Seen & this = Doc ft ADHD. fo children. SOC28COHCHTROBOEO8HDOOES = pe is @ Smulant SCOOKHHOHHTDHHHHHOHOHHOHOHHOHHHOROE4 i Adults ADHD. ® ° Atomoxtling - lon Stimulant Doc Foot e ° e ow A. FenFluramtng ° oe ing «= agonist, & have ee ye a. Dexgengluraming, 7 Cenbrany acting " st ‘ suppeessing action Appetiaing Se 4. Stbutvastne Cause wt-toss Cause A @ e ; e Antiobesity drugs Anovectk1 Orlistot 4. 7 LY Fat absorption from GIT: by inhibiting Fancreatic «@ Upase enayme + Tt has per wal achon - « @ e a. Lorcaserin: Serotont DB agont é extn: rotonio aajac “agonist ‘ « ' e Centrally acting action on 3- Phentermine + Toptramate + aa 3 - * ap ye NS € & agonist antiepiuptic, e é@ 4 Ribenamant —» Ry FOL | Obestty- €@ 2: Smoking Cessation e @ . @ Not tn use due to Nigh tocidena oy SE € a © %, Receptors. Ce 4@ Reton' Hypotension <@ Analgesia. ¢ @ Drying a secretions ¢ ° Sedation fe Aaxtotysts - € e - Agonists £@ 1! | Dermedatomtdine : é|e : ¢°@ Gotralty acting %. agonist F e@ A. Clonidine‘ , - @ vere dy, R's ose Autor’s fo ¢ Used o& ant HTN @ : Symp: NS © @ a gasrent / rwssorararin&. aes * c Release © @ mee eat a? or ypespotastation e se sot on aC paxCOfleeSesooH 2000801 e€é Clonidine :- Action uw |. CNg:- Central sympathetic Outflow -decreases - Central sympatholytic. Tndfcatfong:- 1 Hts 2- Opioid usith drawal B-Autonomic diawhea i In Dfabetes. 4. At cuspose gor Pheochromocytoma . He Clonicking Test:- a Pheoelnomocytoma., : ve jot 4 Boong Clonidine given cus > J + ver TBP, tumot. release . ob Fans No Pheoehroncedona. Rétenaline ) B Blockers,} By Reaptoe: 4 HR - +e chroootropte Fagglons q Aum Q) Heoxt:- ft conduchuity- Me dxomotnpie Vagus Supply Atrium 4 contractty — +e {inotropic —> venticle Funetfon om My a's not present in venhicle: Ip Force ¥ ContracHon (Foc) rs oe . B a's present in ventricles - Sumpattetia, SS Ja. t carding output wo PoraaynP: ahaty: 3-7 BP ip FOC > Chotinegia have 90 Tole 0° cee release @ Kidney: Tuxtra glomerular apparatus Gils @ Kdoey ——9 ae BR Cana nme mm nm me 2. Ba RIS 3% Smooth muscle > relaxation Cre cause Sm: Conbratl 1 a. RBronchus :- Bronchodilation. B agonist a Ry B Asthma, 2.CoPD- b. Uterus :- myometrium + cats have Ba ®'S RR DD mm Relaxation oj moot muxde-» Tocolysis RiPreterm labour 4a Ritodvine a Ba agonist act ag a. Tsoxsupying, a aA 3- Salbutomol©9000000000000 @ ( So SIO Wem. rere ’ ol, — vosotonsttetion.« Adrenaline ~ Y 0: of, R's he, J BP - ‘iat? By - Vasoditat' vow Ae a, >>> Br Advenaline + o- Blocker B agonist - + Vasoconstriction, Vasodilation occurs. Blocker: DALES Reversal Vasomotor Adxtnaline + B- Glocker: —» only vasoconstriction occur: Re-veversal of vatometor Reversal dale. Ba Receptos:- Adipocyte :- By i] * Upotysts Intfosic actiyity «4 one raed te molecule, ushich Bring about looy “pect Pastiol’ agers Ta 0 tot 9 hak aor effect Segy Buspivone , phenaldopa , Cespivone => Antagonist: I-A =o D> Tnverse Agonist = 2a - 0 to -! ee Be Coxtoline 94888 @) ot B2p SE (pmem), nae ngenist- a 0 L wee EE gnwerse agonist: pastiat agonist >)a Drugs that oH ued to Treat Gronhial Asthma:- Drugs that ae 1. B- agonists * cepending por Th » Le Short aching Long acting * Salbutomo! Salmetevol Texbutaline Fomotero! Albuterol {A Bambutero! Galbutomo! 79 US . Ty, - 2-4 vs Ty Ino tahes Moan Ba RS praent 07 Bronchial Smooth m- Cause aelaxation, Bs bgonists don't Begonists—9 Divert Bronchodilatos Bet 0° fogiecd roy tae a + Inhalation > >> 2 Oral a. Faster onset action Directly act on Bronchus b. Belles Bioavailability ftigh FPEn Signigicant eduction &f ePm Terbutalin, can be gir sle A RRR NaN ~~ mm mm mY A EN &2 o\v r) | e Inglications:. eo or ° e sawn (short acting 2 agent) LABA Ctong acing B25 6 oust ee - e@ 5 i eats Asthma & fo Maintainence only Fe maintan e e (status asthmatieas) e eé ee tp acute asthma ee Reant study - Formeterol mary be, used fn acu a 5 ; e SJE :- e e #1. Hypokalemio. e e 2. Hyper glyamfa ef 3: Tremors ee ee YU Tachycardia, ec 5 - Tolerance Se 2. Anttcholinergfe drugs give 10 Inhalatforal Roult e e &:- Tpatropium eromide blocking Ae 08 , © Tiatroplum @romt act on _Bronchus > couse diac or fotropium Gromide Gronebodilat @ oxytropfum Bromide e6 They axe more eyective fo Cad ; 6 3 Methyl xanthines:- e = Theophylline use fo COPD. = Amfoophylline - Past used 19 Status epiupHeus. Mo-a:- PDE Inhibitors Nonselective Tnhitit an Fsoforms PoE isopors. inhmit op POE s PoE, PoE. OP mie seethytraeibinas Bronchial Smooth muscle have e ee ee e a% ant inflommatory: Route: Theophylline by Oral - sustofo velease Tablets -> heaphyltine — warrow Therapeutic Todex So plasma Wels is Ne 5-15 mgle- = PiSmgle > Toxicity Follow zero Order Kinetica > Elimination get Saturated , Theophydine get Equilitcium % cause Toxicity . Theophylline Toxics TRIAD! b+ Setaure 2. Cardiac axrythmias Cron Fotos usually) —pdaeis’t Cause death. B Resp- Suppression cause deat ter Toduce metabotiso gy Theophylline levels ef Theophyline Falls So RR RR AN Rm mmm ope Pe te Smker cigarette Se Plasma Wels |, Therapeutic Dose a Theophylline Should be t ta Smokers. Poe, fobibitors used io B-Asthrna, . > Selective » cause Direct: 8-ditation - PR Nm 1 Roglu mil last 2. cilomflast 3: Topimilost 4. Drotavarine - Selective PDE but not used fo 8. Asthma . aa Rm = Ackspasmodic dg° | % 4 Corticosterotda:- 2 ee Rous > 3 ele ae ee Aeut. severe Asthma Lv hydweorfitene femisucctnal, e! e e Maintanena of &- Asthma by Inhalation >>>> Oval cortcosteroi e ® Covticosterids ‘ ty can't stop e¢ 1. signfgicant reduction ¥ SIE “drug ate sudé ; e 2. dont vequit -tepering — eaquire Tops e be q dose. = Predotsolone e@ 6 . Hydrocortisone give? = Oexamethas! e® Iohalation stevotde:- fo acute TIO A @ 6 1+ Beclamethatone dipropfonale € - 2. Fluticasone propionati eee ven fatralesiona ee 3. Trtametnowore acttonide > Usually give cutaneous, given fotra ee 4> Budesonide e . e 6 S-(Cydlesonide) ctlesonide of 6. Ftunicolide ef M:o-At: They axe pure aol Inflammatory - Only fer Maintanence. Sle :- 4% visk | Orophoxyogea! candidiasis 5- UUpoonygenase Inhibitors tq: a leuton v ®oute = Oval Use |: mafatanene, dete » Act: pucAint inplammatory Ane divect act™ Like" sterids SIE = Hepatotoyicity, 9 SSS SSiD amount! least - 2 ZopisuKaat 3 Pranlukest Rout - Oral Use ~ only marntanence Act” _ pure antiinflammatory tugs Am mm & SIE = Neisk 4 Churg- Strauss Strdkoee. é a Mast call seabioerns ‘ Inhibit dagranulation q most cll by Stimuli due to € prevention cot fnglux Cexoeytosis block > most alls become stabilias) é . i € Acta Pure ontiinplamnatoy drugs: é Drugs > | Na chromoglycala - € € 2 Nedoeromi Na - é 3 Ketoti fen- v S € HO Lenxotrine @ O € 1 Tt hat Direct act™ é So used f9 € allergées 6 f Monoclonal ABS ¢ € € C G SSCHRHSHSHHRHHRHOSAOHSOHHRHOHHSHHHHOKHHHOHHGOOREVv7\s ele Dies res cs) 2-Aot tng lammetion. 2b e e }. B agonists 1+ Costicostexoids e| e 2: AnKichoUinergic a. 6 Lipox Tobibiters: e e Rest att @ B: Selective POE Inhibitors B- Leukotsiene R antagonist - eo é enn 4+ mast cen Stabilizers. e e ethy) Xanthing S-rethy | o ee G+ Monecional ABS: fe a) Autocotds. @ @ e+ H, Rotibistamtnes = e@ gf generation at greration 7 ee , ee 1 Penetrate B88 Doa't penehalr 888° d : der 6% generat ee 2-0. Sedation. X Some gf ORE e@ may cause sedaton but e e & central antichotiugie dmugs- x less than rst generation e 4H, = @ Mpeg induced Parkinsons disease. . @@ 4 . 7 poirarau dus 7 cool ta te Promethonine , Ch? Orage of aT in etizine | Terpenadine. 13-Astemizote- ee 4 in 7. meclizine 2. Fexogenadine- 6 F 3B Catvfaine - °e Avoided "9 Occupatonat tale @ 4. Levotetriaine - e 6 coer 5: Lovaticline ef 6. Destoratidine, ef F Rupatidine - Yeeaor eG 8: Olopatidine * eG 4. ARelastine ee to. Mizolashioe- a @ e ih. EbasHne 2 Aevivastinea: Le a. Allergies t 3 Anaptylactic Shock: ‘ 4. motion Sickness - é 5+ Prusitts - é tts + +. Chiospromarzine .C Typical antipty chit : Hs t- Doe: |. Intractable re eal core PruxiS not treated by H, Antbistomines- 4 é 2. Tntractable hiccups Doc: Chlorpromazine: fl é Sexotonin ‘ ' ’ te have 14 Receptors. to human body . Sexotorin @s ~ SHTSRS pad ‘ ts ton channel AN these R's ove G coupled ex@pt 5HTg—peobich Ss é Proteins € Serotonin s + € fog on Sexotont : Drugs ectog 9° LAN ~ 4 7 Pw Blood vessel Ack 00 ST ahp Praent 09 @ — cause vatoconstiction € € I a. Triptans: Samatriptan, woctriptar ete ae SMigtip “ne cause vasoconstvicion € Efgectve in & aceuti attack 4 Migrsioe € 1 Sumatriptan => Sumatiptan:- Boe. tripta ¢ Phormatokinetica :- ¢ O- Ora) Bisowasiavility — only IS) , ( o- Sfe woul = Adv Bioasoilabliy as high 24 qFh POO K9SHOHHHHHOHHHHOHHHHHOHHHH0H00888008 0G 4| @ > Triptan has higheat Oral Gioowailability is ~ Navatviptan. + > Triptan which has highat PP@ - Eletriptan - doesn't have long: disration = FTovetriptan- longat oluration g action Contraindication:- wean 1 Aoy Cordinvaseulay Useasre eg: RAD, Coronary., Cavebral disec 2. Epilepsy because they decrease threshold level of SeFause - @ Exgot olkaleids:- rows Fungus + Exgotamine - Ergometrine = Methyisergide - Methysergide - Don't act on 18/10 @ , Rest alt act on Te /t9¢ oponists Tpeut attack y Migraine. agyPpA— Ergots cause spasm [methaxgio -> methy) exgomet vine) Bromocriptine :- Dopamine Agonict Ergot Usedl in Parkinson’ dice e e 6 e e e 6 6 e e oe c e e e 6 6 e 6 e 6 e Poperino & Ergicorol- Noo Oypaminergic Used to Parkinson disea Exgots/ Bromocriptine ting, Diawhea . Causes GT Symptom — nausea » vomiting fa extremitian, 2. Tingling & numbness 3° Tochemia > gangrene|. Triptans - Coc - Sumatriptan 2. Ergot alkalofde excepts merthy Sergide - 3. NSAIDS - Rx 0 Migraine fn pregnancy where Teiptans zg ergo axe Contra indicated 2 HT Receptor a Serotonin: location + CNS 4A Poxtiol Agonist at 54T,, © / \ } Busptrone- 2 Geptsone ail are used 19 Anxlety disorders je 3: Lpsaptrone- Pottomriedy drugs: 3. B ST ae © 2 Antagonist 8:- 1 methysergtde - exgot alkold G'sje - Retropesitoneal pibresis- a. Ketanserio:- used to Raypouds phenomenon. 3. Cyproheptadine tf Post gastrectomy Uses:"3" Dumping Syodrome 3° AppekG. sHmulant b’eog gy 28/2 block due to this not ated Aourande aan A DX BAR OM GR DR PD mr Hr D&O A Mm Am mm m HmLy SHIT, Receptor: Ton channel. = ‘AcHvotion a SHTz@ Cause Vomiting. | 547, > antemetica Antagonist «.4.Ondansetvon —> P0¢ ‘I Chemotherapy foduce vomitin > DOCH g. Radfotherapy induce Vomitir 2 Granisetvon :- 1. avaitable as T/D patch CTransdernal) Ginn tye B-Palanosetson:- highest @ agpinity. to SH, @ 44 Alosetron :+ - Doetn’t have antiemetic. action Drug approved Fo IBS - Olarrhea type - SB, swt, Receptos:- location: Git mon: Tt GT mottity. > Proxfnesis . SHTy Agonisic “S Prokinevia —& = Constipation expending i éPleria ‘ wo athe Casibe egr 1s Clsapride. - wtthdraun bjcor gy @7. D> Torsece 2: Mosapride - Not used due to high sje 3) Tegaserod - withdraw bloz a highiocdene Cosctinvasculae events. 4 Prucalepride - Now-a-days using R, + Conltipation predominant 78S= @ They have potinglammatory action by fe 1 PG synthesis by Fobibftion a szume gente ¢ 8 ¢ @ é e Chemical strudure: Acaty! salicylic acid . é e Rou, + Oval ‘ e = Oral Qout. is fort at good even io ents ME g : aapixio given in oral é e 3 TY: ISmin (Rapidly metabolised in body ) é e@ a e “3 puration- lo-tydagt because it ts a Treeversible € cf S jo -19 doo é @ > SSE t.0° ° SHIT WROD Drugs: nea _ fe Drugs which have Short Ty, but long dusation. gy action ¢ e £4" — Monoamtne oxidase Tohibitors - é ; Omeprazole. All PPL'S é © € G uanethidine - ; e Resexpine- : e £ @ Asptvin. € le , os € @ => Aspen USes: Dose use. Tinoate nt — ¢ © a 15 - 325 mglday Anti platelet action . Clow dose) C dally — 45/150 roglday ¢ @ . aa e a 600 - soomgldoy Analgeste 1 antipyretic fb» : i @ 3 2- 49m] day Analgesic, antipyretic, Zp © antiingiammatory. « @ _ @ e @Indications q NSAIDS:- Antipyretic. < tn Pur. via) vi~ @)}@ = xy Aetfong | ° le Analgesic <- In pato ee Antiinplammetory.<- 2 foglammaton i 7) Se : e: NGAIDS, [@ 4562 + Nausea e| x PS production —> Gz ulceration e@ Vomiting (prodsigeato el bued. \, ee Hasmatemesis Meena. Diaxrhea . dec - More ee 7 acute ued be “ore e meet » PS Chronte bu ee. ee @ e Md Sevan Ne a) culoy i+ Noo Selective Cox Tohitttos cauge Ineriace busding @ é Selective cox 2 © 1. T visk ef thrombosis. oe) a tmz. ee ©@ Rofecox' NSAID Withdrawn dus to P vick a MI. °e All Rina! Se combtoed e Dijgerential hagensts of > Renal 1+ Analgesfe Nephnopathy 215 ot. Renal paptnary Necrosis e @ Phenacstio - Pagent drug oy Pom ~ uithelrawn cus 7 ich o@ Coonactmely 6 Analgesic Nephropathy . 6 . eq % fiver: An Nsaios hove Hepatotoxie se Aspivin — Reyes Syndrome :- 1. Aculi fulminant hepatic fail é 3+ Encephalopathy PCAES ove commen tn children whe Sugyeing “from ufral ingection 99H BBS¥ ied Nasal polyps. — ethmeldal - Allergic Rhinitis an @% them Caused by = Urifcario. NSAIDs but max: by = Bronchial Asthma: Aspivfn- = Cox 3 Tohibitors :- Poxacetmol < but don't hawe, inflammatory u axction-C Poo) analgesic, antipyrete- -» Tsoiated For Dog brafns. . ‘ out ony a remat YS > Acute Gout 1. Doc - nsAlos ut becouse _* Aspirto emsatod contratodicated fo Go acid ‘retention ontitoF? te may cause oes ne 4 2. Colchicine: 3. Corticoctenotds = Colchicine © sje. GE Symptoms 7 Rhabdomyolysis- Doc - Fomilial Mediterranean Fever mH Pa ant as a a a ot ee a mh DNAaA Aai « 2 e I e Molotanente % Gout:- Atm to v Urieadid. so © @ 4. Tobtett synthuts 9 Ovle acide. ee e Xanthine e e Kovidare . e @ Ove acd e : ° a. f usoary exeretfon gy Use acid ee ; @ Ute acid can be metabolized toto Allantoin by 6 e Urati oxidase, Urfe onfdose e i i e @1 tohibt the sii Orie acid:~ 3} Drugs tohibit synthesis of ef te shore © 2+ Ege f ee Xanthine oxidase + &g> © Allupuxings > Sufctde Inhibi CY) xanthine oxidase © ee Alloxanthine. 7 ce) ‘padiive metaboltte &6 Coxy'purtoos) oe oyeloonygenase 1S Suutetde emryme . e oe > Ailopurtoor is not a prodwg- ee > Ty — 24-Zohrs- & > Te ts on 4 drug used in chemotherapy Induced & | & hypesuritemia,. % Ha -Azan .|vis % > Te ts one qf the Orally active drug Zo Kala Azar viscera @ Leishmania & Ses. b Rashes / é@ 2+ Hgperseositivity Reactions @ » @ a @Shoiter acting dug tT §-thrs = Over all reduced indice focidenee Y se Tt utnasy exereton. of one acid ka Uricosurfe action: dhug toteraction t Pencitin Cydlosposins - G~> Probenecid »- Urieosurde drug. Gre acid metabolism. add. . Takin L— Recombinant Use oxidase — Ras buricase . Cfrom bid 9 A 3 Doe FA. Tumor lysis: syodtone. > Rapidly metabolised In body So it bos Sbot TY. Payette gro > 10 ‘nereate Ty, - PEG addsd ove acid oxidase . _ Pegloticase Clonger acting) 8 a a > ?PPB > b Duration «PEG bind to plasena proteins auton. - Prostaglandin et Z PGE analogues: |. misoprostol ®t HEAP toddcad pepe alcer- [% sed fot. prevention Hey Pepe ae D> Specific fa Nsmid Induce Uleer~ misoprostol: 3 a8* trfnester MTP TS pry Analogue - ay [+ Exec. dysfunction a a a a a a a a a a a a3) Drugs fa evectile ayspunction:- (-) 4, PDE-5 Tohtbitors 4 PBE-6 © » Sildinagi! Cwmeaay 7 D0¢ as Vardinagil 3: Tadalafil 2 PGE, Analogue : Alpsostadil- +, p's fi a 3. Apomosphine. — act on morphoid opeld &* fo CRS ¢ Oopamine agookt 4+ Bremelanotide. —» launched a4 Taming agent but now used os éD aug ‘ \of HTN 94 SJE: ys witha dus to high fncfdence a > undsr evaluation For Septic Shock. > PGE,: kin Dinoprostone :- Ripening 4 Cervix prioe to labour inde CCerviprime ge!) 2 PGFoe Analogue: I> Dinoprost :4Pq used fot Induction y labour 2» Coxboprost:-4" PPA SC9OHCHCHHCHOSHCHOHKROFOHOGOGCCAROEE 22908 CC7OR2HR02 0200200 4+ kotanoprost PG onalogues 2: Fravoprost ted in glaucoma eee eee 3: Bioatoprst P uveoseleral Outflow Coquusous) 4: To glu prost D> PGT Prostacyclin analogun \- Epoprost enol ns 2. Treprostinil used in Pulmonany auteval 5: Ttoprost: : . Copp's? . 1 Ca Channel Blockers:- Dinydropystdale >>> Verapamil @ Diltfa: 2. POE, APE, © :- Sildencpib, Vardenogi, Tadalafil. 3: PAL Cprostacyelin analogues) * Epoprstingl, Tre prostinil, TLoprost- HD MD A 44+ Endottelin © antagonist - Bosentan mold dug Lnonselecive Ota € > 76) seective © = Dasugentan = Sitaxentan - eldraw Seon hepatotenity 5+ Soluble analogu. 4 Guanyly! Cyclase b Unaciguat - a. Roctguat- All the 5 ate Vatodtlators AE Om ANAM mme@eoeed @000 0 4 @eee00 COCO HOESECEOC EOC ORB ERO Be Cordioveuculas Syste . eee te L + Drugs - For Conguative Heaxt Failure: + Diuretics 2. ACET & ARBs 3: P-blockers- Drugs which have Ave Trotrepie action. 5+ Nitvolis 6. Hydrataaine - 4: Traditfonal medicines spr aldo fe Bo: . 3 le es Fot Aldo fn tate Der 2 . oare Cortical comecting Cy Ind — Uk? =2e0" Chick attundiog ink LM) + Bede tate OT - Lass af late Det - K’sSpared Any diuafic that act on + ofter Late Det > conserve ie diuretics Heol Major action aq Osmotic Auretics ip Loop YEaxly DCT _ a _> Merrninas oor pidostoone® Wg Garoiateral elt AN Ciuvetic Aldostexone Present in > 4oop + Thhanics combination - mp to Thick ascending xequire access 1° Tubulas lumen. except which ad from aft sae R's one © antagonist cegtopiaam of late Det: Loop x Thiaaide Diuretics - £0 mb % Loop & ae provide Syrexgutic activity y all others ate oddifve ———_ Lateder Ni + tna nal at => Moa eouty OT ce th Prevent No. lass tumen | EM from body 50 tt reabsorb NO doesnt . Traditionally Coune hyponatremia, oi 30 Loop 4 Thianfdes Hyponatrenta, fe occurs tocase Y Overdose * AN diuretice S urinaty No ™ Loop & Naa couse => hypokalemfa Thiaaides hypo } na obempl. 2M: Alkalosis >? hypotension > hypotagpesenta, CA ovnany mg) Loop > hypocalcemia Okeabsnpten) ‘uring Thiaridis> hypercalamia urine a ae 2 PX RR MO m = aeb> eye wep mene 7 4 ° (© ttaatde © > eaduer Ca. a 4 Fovmation of Renal stones: So it e. : ee fs used 08 Ry fot Renal Stoner. _ ° e e Of Thisa‘de Diuretics given > B + ° : F ays #2 hys:- Tt Coe Paradoxical P urioe ca apte e ee than J ; Ss metatovie Effects !- T ipi tr gh 76's eo ® _ hyperlipidemia a high 76 id = hyper cholesteraumia, ' os ~ hypexghveumia e& = orienta - e©e hyper ® acid. ee ~ Loop Diuretics cause» Otototae <— Ethacaynic 00 ° set @ . > Thiarids © doent cause otototicity- e i 6 > Thiaride Diureticg SIE 2b Evectie alytfunction jen Loop diuretics. ° . 2. Impotence - e® Tnolications:- em 1) Loop & Thiaride used for Ory pe % a ni tantdes - 48h Une & Antihypestensives. ( Thiarids - 4 . a) Both One nf PF — 3-ARB'S 2 3) Thiarider & > ' Renal Stones @ Nephrocalcinosis & Nephrogenic déabetes fosipidus (wor) “ eae) oO Qin nor Anticiuretic due to GF Normal — Diurenic aan: x 8 + Spi cone S |- Sptronola . Te = Oral Bioavailability (F) - Very Poor because 4 qe Very extensive Fem iT «@ « e@ Indication: ‘ - CHE — re usitt wetard disease progression 5 fe Q.HTN - gt is used a4 adjuvant T Loop a Wold’ ¢ @ to prevent hypokatersfa - a e é e Mane ° pdosicore cause Na U Hao Retention ‘ ; kr a nt loss - ce BSHmuba fot Aldosterone is hyperkalemia. ° Tumor tn Adeeng! cortex ee Conn’s syedsome HTN € @ fest [ie i: M-atkalosis é @ SJE - Hypotension ‘ \ Mdestesone > NOM Horrexntioe On @ 2H kal mic é a Aidocrexone ® Antagonist > N% lip loss, e@ 3: M. acidosis: athpes é |e i our € @ 4. Gynocomastio cs fot fog Teatosterone RS. pre tortie s: Teopotente, By blocking rex! ‘ ° 6. Loss | Libido : e e Q. Eplevenone Spect gleam block Aldosterone ® «3 = gelactive bios aldosterone © ae Epkvenone >> Spironetactone Z e ¥ docan't caste Gynacomastio €@ e e @CORES CHOCHOKGHOHOHKBHOHBZOO4 CCCOTF7ORF AHMAR O COOL Carbonic Anhydrare Tobititors . (c-4:1) a ae HEE He Actorolamida:- |. RinGlaucoma, Cneodiuretie ute) mon 1 production of aqurous humor: = only Systemic prepavatfon Dszolamide Reforoiamtdes (won Compelifive Remar stole, NS Aotagentan) Topical administration 2. Epiupsy Catamenfat epilepsy 3- Acute mountatn Sickness. 4. Alkalonize by Ustne by decreasing Bicaxbonatfome rab! Normal hen | HCO, veabsorb NH, get excreted Jn. C-A-T, come Hoo, — lees NHy — Ruta‘o v NB. 3 aA a in liver Vv Liver Failure pts Ni, ciposite Hepatic eneephalopathy davele = Hepatic encephalopathy COAST GntraindSatin 1 KY Sparing iurete ' poe in Uttium induced Diabetes To ‘dus. 2 Prode symphmate releg to Cysife Fibrosts)yMarnttol :- 1: PE: & Corebral edima cot) tn Tb LcTensien. pts- 2. PE & acute angle Closuse glaucoma , which causes Jf Intra ocular pressure cfr: [Pulnonaxy edema ca ? intravascular volume : Y 4 vinous Return t & dy Ri abun uit stretch 40 Accomodatt. more blood 60 so Rt: atium has Stretch Recaplors woth regtex Seeretion e cause endoginows tn : 2. BNP ° eee 2? diuresis I] cause Reduction 10 totravascular volume - i awe & Anup. Jn CHE , 40 4 Volume , we have to use agenisls 4 So + y ANP > Coxperitide 2.1 BNP» Nesivitide sup onalogus, Nesivitide = - recombi - given at ify infusion because pant BNP aoalogut - af short TY, = Resewed for Acuti decompensated Heart Failure oe eS Gg < I ANP 7 yoturesis — by acting on @on medullary € « é ‘ € « 4 4 € «é ¢ ¢ € € & € € ¢ eB COCOHOHOHOCEOOCOOOCOQOCOOOOOOOOOECHOK9HCHOHOHCHOKHOACHOOHHOHROO4 SCS SOCOODARAOED OO Neutral endopeptidase - enayme metaboliae ANP & QnP. b => Omopatrilat —> 1 Qual fobibiter og I Angforensia Cometing ae 2. Neutral endopeptidase | ome Ror asad ™ 3. D Angioeduma.. 3+ wldea due to T risk &Y angioedema. tundis Tria! Coty. Natrtuvetics :- | Omapatilat a. Nesivitide B- Caxpevitide - System. CRas) Drugs acting 29 the Renin~ Angiotensin System RAS = 7 BP when YP Angiotensinogen v deni > TG al secrete .CTinbo Gumerde eas Geils) Angiotensio-I Car-1) +BP . | ro AT-a L y Qeuptors s Short Ter Long Term mechanism machanism 4 Intravascular volu: ue > Dreet Vasoconstriction AT-B cause Aldosteron Py gdvesel rea Release Adrenal center v Der vu ‘1 Nat] rab L f Volume Lat@ Block on AT-T @ » ARBS™ fm AT-I—K aT ACET @ Disect Renin Inhibitors AUiskivin used ab antihypertensive - => PhasmacokineeHes gy ACEI 5 AN ACET ate prodrugs exapt eacept: Captoprid— a-4 hrs + Listoopyil & Captopdl. oTy - withs Shortat acting Acet mpigEnctapett TH. $ captopril ™] TY_, Enalapril < Lisinopril. > Use HTN: = (48* Une) a CHF g 3. MT 4. Diabetic nephmpathy poc- cet 5- Scleroderma renal crisis. Ares SE 4 Aut k SNe Ae hypotension a MSiodtiaKon” cause postural hypotension acer cause | close effect: 3. Just Ure Praresi 4. Duwetics + ACEI AB's A postural hypoteasion risk, S- Omission of Priev diuutic dose Lb wiek & Postutal hypotension- OAT TA mm mm AO Mm Mm POCHOCHSHOCHOHEHSHHHOHROGHHTCHHROSHEOOHOHROEOOHH OO’wir ak» hyperkalemia, metaboltc acidosis . <— H" retention 4b ee eo ¢€ Olveck aldosterone antagonist — Spironolactone, ee . = ’ a Fndixect aldosterone antagonist AcE, Aeak e e @ 2 Beth can cause hepatotoxicity @ @ © 4. They cause Glycosuria e 6 ee S- They Cause Dysguesfa. Cmax & Captopri!) © GS Thy precipita Acut, Renal Fasture. 1 move fq b G/L renal a sh e . “ 5 e 2. Rena’ a: stenosis in one Kidney . @ e ‘ , © 7+ Pitlded to Pregnancy been ey Teratogenedty, couse e | organs. Cme is lunge > ee hypoplasia q Fetal ong oo a ee AcE present tn endottelium af Pulm: capinanies ee e {king i ®e Brady kinf eluvotion Ace © —>feradykintn® Dry cough muta botism oy bradykinin © e ‘g) e 6 A ngioedema, pt. & ACE® develop & there S/E , then e e R ashes Use Aras Urticaria SAIN STATIONERY GAUIVAN NAGAR, 046546 41324 © 9 811982849 aoT — Non Seective Blockers B, Selective - Blockers _ Resta, Carvedilol ete. > fi — B, Blocku selects & additional actions D generation: ER mR RM COCOSKROCHOHSASHHEHHGHOSPHREH9HHOHROOHOOOE ast . tL gueaton i I nie - Metaproto) P fodolo! | Atenoto! a 5 es ees - Acebutolo! ccaial = Bisoprolel = @somolol —Shortat acting é Tia B-tomin ¢ Duration 15-20min, eve Todfeaton Y B-blockers- ~ spur nee Fottaxe. 2 Me (netrophic > y Contratiity. 4 €f1in|- Cong: Heaxt 2 Tn CHE 4 condine function veduced sb (as compensatory mechanism) aA naEOn en Remodening- yo ipindon (short tern) > dite to heath shonege og c oa povertieulla Za. long Term Patton worsens dust “4 e| = ft mortality é A . r fog : PAT - 1 € block by ACEL Remoactiing : caused bY ! on ‘ a Bt p-ooceas ¢ iy long tern, mortality ia decreased Ly v sing ACEL « BO , Abv’svate t et at STATA teeta COCO OCBOCOHRORAOOOBOOOOS NYHA guidelion:- “9? ae OT . . |. B blockers should be started at lowest tpective dose. Copttmal > (ose Shouldnet 2. Dose to vet gradually Wed 3. Only Metoprolol, Bisoprolol, cawedilol B blockers are to be ured - 4 Cautton should be exercised fn NYHA Class JW Csevee stage con use fn Class T/)@ NyHa Cixet Heaxt Failure 5: Tm acute. decompencated Heart Failures ogter stable person, beter to be Ry by Diuretics then ux can use pr Blockess; $0 x bY Ei ‘ avid in acute decompensated Heart Failure p biockers fot only Present in Bld vessel. to other site also. a. HTN: ” © p> Lome q Contraction (Tn hase? Blocks, L ve Taco J Cardfae output Tot peiphnes gh v 0eP vu sBP @ B,@in kidney + Renin welease . B, locker J Renin releate 3 RAE systeo + LV GP- Me lol . a 4 woe prefered aantthy pertensiet Atenolol @ pO | conduction C-¥* dromotrepk action) B Blockers as effective i arrethnics , more eppective ip Sventteulet Aiythmias - 4 Sh auythmia start from otium pass to ven hich was stop ty pO4. Angina 5. MI becouse ay fonibitfon Rernoduiting . oo Dissecting arttic aneurysm + Hoem Sle Pr Slorkers | =ve cheonotrople Bradyearaio 4g. eve dromotropie - AY block, —> Hest Bwek- - precipitation Y Heart Glos Failase to 3. —ve lonotropic avna Go 4. Hypotension oeeajale Vaso 5: worsening the toterentttent claudication > Bmediale conser v PyD cjz- 1 P12 heart block. a. PvD @eee00 @CCH}OGSKRHHOSARETDHHGHSPH9OHOHHHRHORVHCD @ 3. Bronchial Asta. ticor 4 Pe Use already antidiabetic dug neh a By blockers they alse cause bhypoghveeia - covery fr hypogtyumia . if we uke B brctars taskad 9 antidiabehio 4. Diabetus mellitus yamia « Hoe He an aR eM a mm mm mm mm — mm om nanan a oa... B blockers ust day * pee et . eat a B blockers not only present ia One Sil but also offer site, tt, 1 SIsy@ act? of adrenaline 00 BQ Ly Bobioctsrs mask S/sy a adrenalineae v|\|e ele Effect Y Adrenatine fo Blood glucese:- ele 5 ! e A guucose / @ enw“ guucose db - Advenaline velease 5 which Cause output 4 $ e RR, gucose by activating glycogeoolysis #0 hws e@ Ae Peeinietnied by Ba, Receptor: on hepotory! ee Bacogentys e@ Adwenaline a e 4 Ba *¢cpto 6 Pancreas B calls of Panereat Contain co" " e Adrenaline pdnnaling . t 5 Ke > FO + QiMcogendysis eo & \ aé ouorn | ia ee ~ glucose, ate J tnsuttn secretion —‘T Tosulin Secrefion ®@¢e & mediated. e A Adrenaline :- UY Insulin scexetfon to T glucose . e e in Panereas e ee =>. B blockers act on B @tblock Insulin secretion | So 4 glucose 3 ee which is “very minor. e6é ee Major action is on By Receptor - | @ e B blockes e@ v ef 2.® of uy ee Ueglucose Chypegiycamia) eo ee Z ®e3. p- Blocker C/T dus fo hypoglycemia, poistently. “becamye ptt alteady on haypoglyeunte com. Non Cardiovascular. Conditions whet “Borers uuedi- Noe ON — Benign essential Tremors - }: Propronetol:- I a. Antety. Cstage Feo ~ Performan) B akathisla - ( Restiess ness) , Gq. Migxain prophylaxis 5 Portal HTN e fy Somatostatio /Ocheottds G. tehitt Ty? Te ued 10 Thyroid Storm ot in acute thyrotoxicosis - iF, Glaucoma - Timmdol , Bitoxolol axe used, which Y aqusous Production = tve Lootwpic action => Based on Moa 1 Candiac qiycosides oe digitoxin pee group dligaxio Duving 84st cut hoe to vetract for Tis, 2? enter from outsids te inside. Ciastole., cot has 40 ge outside by by No /ca%* antiport Gg win « TN mm & @eoo0eeo Veoceee e @9ORHHOHH9AHGSCHHHHPHHRHODHSAOHHHOO a Aa mm oe Ana A active Transpat UAn ca%* caslt transpost Outside So cot -that is present fo “S| Caxdiomyoeyte Stored in Cot that enter into cell’. xelease Cat from savcoplasma vetHiculu Saxceploima ‘reticulum . SERCa2a which is Calcfum induad cae ¥tlease - a pose 1. Refieulum ye systole car enter foto cytoplasm by Po 2+ Gytoplasen 3 tar) Reticulum a extracellular - Cs. Extroclul Diostola. ca* exit Into Reticulum & “ extracellular from cytopleim - act on Not—kt atpase Digoxtn J 7 tach Na" outside k* toside . “ Neemalty . Effects ie z fects Digoxin: Bind E wot-k* areas U bock So Na aceumulate fr call which cause * fobaceltular Not nat [8 Aap 1a" takibition y wae! antiport [tail Re iobitit J, 2 ca? accumulate thetde cell but io fatto. co™ cleposited Fa : ¥ . ich veleane + Gilplatm so” 9? actvation ay SERCA2A So which aa CHOPCHHOHOCHOCHOKBOCOCHKOHOGHOOOE 5, f intraatulay ca stores 6 > MT systolic ca in cytopiosm 4 Fors 4 Contraction (Foc) a) ele erally. nilea t wot hich is sevens! 5a @ CondifinContraction + 4 to fotracututar No lls, resulteg to revexead action | not-ckfexchanget, which ¢ oy | Rormally expat one Snbracilalat ¢ Ow SERCA 20: we Cot fon out of Call X imposes pratt = wee 3 extracuuias wotions toto ce. some, UAB st é - dusting diastole . Tat enters toto Cytoplasny & Cause areythmias - & extrasystole. - Rexow Therapeutic Tadex So TOM Is needed - é € SIE :- |. GE Symptoms ¢ 1 Cavlat symprms- Nausea Vomiting Diarrhea € 2 Hypexkalemia » é & Digena € . Ak ta outside cell. B-Wisvagomimetic. 50 ¢ Bradycardia - an AF, MS, CHF, RHO, é 4. AN Block. gP u pulse v e Bradycardl - : 5- Yellow uision due to digoxin totexfore % function af Cones . 6. Gynecomastia ¢ 4. Areytomias - C C ¢ & e@e0 e COHOSCHHHHLHOHHHALOTHT HH FO HOOHO HORE OEC9OGHOR89CHOHKBCHOHHOHECER @eod SOS8FFHA MAHA O00 Factors that Precipitate Digoxin toxte nr Digoxin — Pump biedio’ 80 hyperkalemia which acts 0s & Negative . Nd] atrase feed back on Digoxin Cprevent tontdty Ter : ele ao reduce bie Digoxin & . leckrourten edting digox Pump J HypoKalemfa: becouse 04 Lose ay ve Feed back regulation, 2+ Digoxin + Drug causing hypokalemia ( B-agonist,Olurtfcs except spirinola: Amphotertein 8 ) 3 Hypexcalcemta ‘co outside - 4. Mg Cprysioiogle antgpn'st 4 ) J (Plasma) v ypomagnesen’ - gradient © vu *, Srtroaina cat v Drugs at leakage % cat 5. Quinine . -— oy U Renal excretion of Agro, ceythntas - tohich 1s modal excreted by Kdneg 6. Exyttuomyeto , Tetracycline Omeprarcle. » Y hepate metabo Uism a Oigitoxin- 4: Verapamil & Oildiazern we P- glycoprotein inhibitors dus to thi, they precipitate: toxicity % Digoxin + Succingdchotine > BD visk Y Onythmias (Deporarising nm blockt) G. Renat Fatuse - excretion reduced 4 digoxin to: Live Foftue — metabolism a digitoxin Reduced \“kt supplements Cause “1 Pes haxing —Tacehyarythmtas vatoration ey “Vt Fead back » ' Propronola) 2. Svenhfeular oxrythmias du to ; B- AV Block Cvagomimetic action) Rx * Atropine - 4 VentBeular ” axythmias bys Lignoeaine Normally Ventweutar arnythefas — DC Cardioversion But in digitalised VA > Oc Cardievesion\ts C/T dust precipitatio ventricular Fibvillation 5- Ankdot :- Digivind (tmenoctona.| 8) = Umited availability Catecholamine Inotropes: Catecholamine IQetepes: je Dopamine. pose Ma/kginto tM Mopusion Dose - Aeiton 20 mam Lowy 2 % af SSHSHSHOHLOHFTHSHEHSHHAVHHOHRHHRSHHHOSGHHHHOVOCOE Jotermediati» 2-10 —> a « igh >lo a% 9-5 7? Inotvophie dose Le gradation af Response sean fo THE range ony a am mm mMood ee tooo oo eeeorececs CSCC A8 ROH O00 actton on 8, 23>> a, 4 velatively, 29 High dose % 2efionseen Pi selective : Therapeutic dase 2. Dobutamine >- Dose - 2-8 g/kg |i Z]v Togusion- Catecholamine fnotvopes Ore used foe Cosddogeoic Shock . Dobutamine > Oepamine Calefum Sensitizers CARN ae Heart Glood essed Bind +e Tropanin-C Direct opentog &% 1. Levostmendan. (4 which bind Ca- k* Channel opener a+ Pimobendan- (> t ca sensitization. wv ‘ typerpotaxised vu 4 Fore q Contactor peeeee v . Nasodilation. Inodflators:- Levostmendans & Pimobendan- yses i= f Acute decompensated east Fasiuve. CL, P 8 siseritide) 2+ Pimobendon ured tn CHF fo dogs. Duo! Acting Tootopes: Tstaroxtme:- 5 Not /kt Arpase tobibitt SERcA2a directly > actvate fr ona decompensated HF > Tt is unda Phase Wt 4of pre, © . Tt cAmP ea queetel Heovt Tv (Sroosth vetnet) woe v CJ *, Contraction Dilation * Inoatiators! Inodit ators +, Tramrinone Milefnone > Toamrinone (potent) a OM A OR OM Mm mom H 3- Vesnarinone - 4. Enoximone - Route NO oral eon ass & T mortaliy = given tv. € « ¢ > Tnarninone short eases ; Ty, - 2-Shes 7 > miltnone Ty, - 60-Bomio € Shorter acting. € SJE» Trangient Thomboeytopenta ‘ " Short term management gy Heart Failuse . € € G ¢ € ¢ ¢ SOOHHHOHOHCHOHS HOHE HHOHOTOHOHCHHPHOHOHHOROXVOCOE‘ s Angtoa Pectoris Manifestation of Cardiac tschemta Cu blood supply) Rei Ib PO, Supply. a- 0, demand. 3° Both. ‘chr, variant.) I. Nitrates — Doe For alt forms a angina. . C ¢ 2+ B- Blockers o® 3 Co Channel Blockers: Nitvalés > Dilatese bothe Arteries and vefos but Veno dilation > Arteriad Nenoditation v sbvenous Return v v Preload. v Yo, demand | > nitrate cause Coronary a- dilation 20 load stow 1 (2a Suh | S9OKBSGHCHHGHOHHSHOHSOHHHOGOOA eeleOFCAGH OAH ODODE > Nitvalis are No donors u Guanyiy! cyclase v Teamp zy v Vato Blation1 Rout. + can be given fin ang route. 2: AN axe long acting excapt - Glycry! tinftrate (et)NTG ds Shore actogs 3 All Nitrats Undergo extenswe FPm except Tsosorbide. ge ‘P mononitratt- SJE + 1 Throbbing headache - 2. Elushing | Excessive Surating 3° Y Hypotension - fy Reglex Tachycardia VBP activate Garor's v 5+ meth Hbnemia Reflex Tachycardia (nitrates + HD 6 Tolevance Dug Interaction ct Nitralis + 1 Gildenagit:- + nitrates = No donors v _ additive hypotension: C[t to heost Asease _ MI visk a a a nA AAT Mm SOHOHCHOHCHSHOSRHSHSHEHHOHSHOHOHRHOHROHHHOKHOHRHOHVO DOErock, ca®* channel a nitrates coue. 2. Cer (dus to b preload) 43 To prevent ‘Recurrent Pritaemetal Angina -Dec fs Ca channel (cee) But fo Prinaemetal Angina — Doc - Nitrates » 3+ Nitralisatso welive Bilary Colfe & ESophagea) Spas 4 Gd vesse1 by activation Y guanylyl cyclase - Spouse nck 2. T Type cus °'* Cp0e) ee Rete be Angina. Doc. ee oe @ e ° e e @ @ @@ ee Se @ e @ of ef ee @® Classification :- ee eo 1s L Type cep ge cvs e° @ L-type. Ce @ ae Verapamil Diltiazem Predominant act?oo 4° Meth-Hb + cNat— so used in CN poisoning acts at chelotot 2 Calefum Channel Blockers. (cca) 3. N-Type . cus. ~. Othydropyridine CO¥pin) Heort @id vesser SOS" | + L WW Force q Conhaction welaxaton. Lv v Cardiac output Vatoditatfon L Csystotied 0 YP Cveinstropic eggect) vep L v hypotenevon. & O Reflex Tachy oo Beocycatdio © hypotension.Intecactons: AV Block, occur by UFOS =F Verapamil & Diltiazem even) Se :- p Blockers ase cause. v 2 Otgoxin Ay Glock. by. Verapamil 727 Diltiazem & € ¢ é é ( 1) € € hu Svub cant Combine E Bp Glockas thet Perelane 1 oh combine , that is € dapiosiets Bbc > vuDd + Digoxin > ‘ € Precipitation oY Digoxin Toxicity ‘80 it Should not be Gombined eva, € € to Bo blockers Fe ~ YE chrono, Dremgl => Vv Ud effect 0° heaxt . € —ve inotropic - ; e/z: oe ccB fo CCF € € User: 1 Angina. é a aTn ; 3. VD we to Supraventfoular axnytmias . * : Lo venhtelar axruthmids ~ Umnited role é 4 Depto — doar have vou ‘> axnythmias due to neg sgable ( act” on heart C : 5 Depins are used 24 Tocolyticn in Preterm labour but not ved ‘ @ SOHNSHOHSHHOHSOHHHHOSHOTFBOHSPHHOSHHHHHEO ROAee ee ee | “4 Verapamil W Diltiazem Depios - SJe- 1. “Hypotension * + Hypotension wi =~), Jain 2. Bradycardéa. a> Reflex Tachycardia® +0 3- Ay block. ( VFoc) 3. Headache Catodfiat? Deping) 4y Nausea. 4q- Flushing 5 - Constipation. S Ankle edema (Pooling b-also cauue Ankle edema but blood fn dependent part: But less. *Ntenadepto + excenent Pass SEB _ used in Cexebral yoxospasm - 3 B: Blockers act by J oxygen demand by wv sympathetic SHeulation of heaxt ty Trtmetazidine = Anti Angina - ack by inhibition 4 Fatty acfd oxidation ia. mitochondya - = NO Cordioprotectve but claimed fo be | Cardisprotectve- ® Ranolaaine :- Mo-n:-[-ahibition y Fahy acid Ox Fatatfoo Be Tahibit fa Solum currents: Advantaga'- 4... Tt dots show Cardioprotectie Nou) uapgradd a, gf Une R Chr: Angina©. + SK’ channel epenessr- used in Angina, HTN gfe ;- Salt Y Wyo RetenflEn dua fo this , these are ot pregore jn Angina & in HTN: . Fk Minoxidil ag fe Alopacios Rout. - Topical - 5%} - Males. ap — Females - 2. Diazoxide 1-8; Tasuinoma . most Recent antanginal drug. tp Tvabracine :~ ~ = dohtbits Funny Currents ke Eypertsosion. T- Diuretics T- Acer @ RAS DR B&O EN MR mM ma A A RR MD — HH A Mm Oo m a fy - B lockers We - &- Blockers: «| . « T- G Channe) Blockers ¢ G- vitvols d A ¢ ¢ Yi) - — Gntval Sympatholyticeele Gobel Synpattolytics. 4b e,eé@ ON es eg te ©) @ | Clonidine | ee . @ e a. metry! dopa - ( Prodeug) ° J e e e@ - methyl Nor Epinephrine Cackive metabolite) ee 1 ee Ack. 4 False neuvotrantmiler °e e SE Auto ABs Form against Racks - ATHA- S Cute zmerune Homotytfe, e8 wei @ ef | ee ae oesletes) Se he 3 mixed ee 4: Preferential venodilators 2 Preferential axtertodilators : as Q e Neo. a>Vv $ - eg- Nitrate 1 Hydralaaine Rest all. a. Kehame openess "Na eltvoprus ; palopore a. ACET . Channel Blockers s Co woepin 3. ARBS: 4. of- Blockers §. POET | .> Hydvalazine:- Predominant > Le Light sensitive So protect in dark bottles. 2+ only Tiv tofusion~ becoure ey Short Tr 3. user Mindicafon — HTN emeegengy . overdose — CN Poisoning > Ry tt Nitrates - can cause axtexio ditator- = very good alternative +o No Nitrprussice: _ nso eggeetive To CHF Fran Fenoldopam:- | Dopamine derivative 2+ D, Receptor partial agonist 3: Re in Hypertensive Emergency f° T/y Foon. fern to Pregnancy Clt :- — Diuveties ei selective A-Glocker Gan wie Nongelective A blocker Sodium Nitropussida Ee» Rematoing alt antl hypertensives can be Gia in Pregrancy , Doc — HTN emergency in Pregnant women is I]v Labetolol CReptace Hydrabaine) BRR ARR RN N/M a RAM ee SCHHHHCHCOHHHOHHHHHHOFHHOHTHHOHHHHOOOOOER4b vis a e | e HTN fn pregnant :- methyl depa which is weplaced by ee Labetolol- ce cu Mmethy! Dopa . e@ Chr- Hypertensive Female , become Pregnant Rye 4 e e 6 "5 ; viene Acti Aexytherta bs e isation) a frag. eporent at egy ®e Prot phode (Rersasteation) 4 e ae e 6 phase O “pha. Reparation) @ © Peptadeatioy got Cattey depolarisation) » Nat co™cunent often 7 —— e (ttt lc deat catty apt 2 Rote ee tod ef Tasave late ud ate Ventiailar Action Potentialtar) + z yt Come dou ee tn phase 2, Amount qf Kr eglux = co” fnplux so A: dows 2&6 e e @ id @> x ) oper Sf > tn Normal , no tn Reding tage jcamele ee wens no [Rak) 7 When simulated Na channel oper «i oe _otet Ate foe ener Skene ee Were File Membrane get depearted | a iz) > srocfvated state - channel open but 6 nf | xnaene ceux: ot toe Toos can't cross e . 7 . efractory Channels at Bme @ Kt oplux of en e 9 Throughout Repoloritabion , aneche Refracdory!: Pedod in hich Gail Rpolarised Sat secur . Reaiing state vecure when besomesOnty Verapamil Dilttazem QT Iotewal prolong « A-P dutation Qe tee 1. class Tq UTe > delay depdarisatton na aAR a Repolarisation Delay —> Class a Class Ty > dov't delay & interval no action on Gep Repolarisaten | > Safe group gy antiawhythmia . > | Ap dutahion ~> AP delay c@ Phone 1,2, 3 —> feactive » ae end @ 3 phate Resting «@ -@ 4 phate — Restieg . « ie : e Classticakion Antiarthythentes:- Ce fe LT ao ve a «@ tT po Al PB blockers ore Class F exapt Sotalol ° i é rE vedyt T ~ © € Sotolal (Bf bocter)-- ge ‘ e - Amfodatort e Sotalol é Y «oe e ce class - I. ‘ ; a ; Ta ,I, biod to actvated stage y Na Channel @ block. & ie verre dilay depolaseatione © Ty, block fnactivated Na Channels dato Repolarisafon. ¢ class iY € @ & @ e e @ e e e e e e@ @ e@ @ @°\|* = dass ii) antiarhy bete 44 e,é : = block K channels — @| @ + ® 6 - Lt Gan also block Wal cot , pRuptor ° é Predominantly. @ eo ® = Slow onset q action. ay groan > ot ce, e@ : ae Ad - long duratfon oy action ee . e6 > TY - 28 -Wodays- ° @ e e Uses + bk Resisting archythrios e sje SJE 1 Deposited fn Comea —» Corneal micro deposits. of 6Ps o 4 * fiat @ G..P- sphesarmumpaity 7 Oepastied in Skin —> hyper pigrentation Wt photosersife, @ G2? rane 3- Cause Peripheral Neuropathy ee @ ee” Patong AP cunatoo 4. Hepatotoxte ——> Civthosis 8 ¢€ 1" teal . Progress to e e © 4,1. tigueotion gts 5 Block Ty 5 Ty Comte hypottyroidteis, Tr Pmodarem Rerfpherat conversion new ed ie tnteracts 5-P - Pepheral convertion ae ys pete Sometimes it also Cause hyperityroicliem Cless) OO op. phetasensitcity ma . 1 = 6. Pulmonary alveolits u fibrosis in which pt- Present & | ae 6 Dry cough °e @ e Cloas Ty wed fn ventricular anny tomniay eVite 1 Statios att: Hg Co-A veductase Mok Act by backing 3 Hydaowy methyl G-Co Reductare . erayime- _ HMG Coteductase action +» Max at sam = Statins ax usually administfd usually bed firmer becaute tt has Short TY & max action at 2-am. long acting » can be given any Hime dusting ~ of statin is day Hmg- CoA : Sle --Hepatotoridty Long TY aenyositis (aka -thabdomyolysis) — ]L:- Growing Chitdeen | Giet dusing Pregnancy > Atowvastatin —ssteractont : Coumavin | Cyclosporine = Rosuvastatin > Pitavastatin.— most potent Dose :- 1-Geglday (lowest dote) se = Sa Myopathy. RR Rm Rm . @S2OOHSHHOHHOHHHHHFHHVTHRHEHVHHHOHHOHOOO4E Ftbrates . Statins + FibrértesC Gem fibrost) Ffbrates> T risk oy ™yoPaty € Stating - 4 ao 1 tn LOL Choksterol ating: DOC in Hyperlipidemia Cmax Fall fn okestero! ) | F}bralis Doc wm. I” High T emia - Conty 76 but Cholesterol Norma) 6 res) ‘ Ture —y Niactn [nicotinic actol CHypolipiderk agent) ; => 4 Chotuterol absorption Drug. absorb cH from ‘ siamo! € wnt ; Tock enterobepatic. > ce K by bei oud Segue Cicerone > Egetimibe Brock @ which a1 nec, ty Chotastere fmug v\i~ eje ™ Pregnancy, No Kypodipidemic drugs ave used - | eo 6 > Roy Mypotiptdemic drug | maternal Cholesterol “> couse Tetarty @ e e > But Btw actd sequibents a used once upon fime . e e a e Children tohibit Cox-1 fm platelets ee @e©@ @ Drugs fohibit PDE ee PoE e Dipyridamok. —> | 6 (won Selective) e Became e i e ae e e foiipratret Plotelet Bid vessel a a oe P< aggregation vasodilation ee +. Miso used fn Angina ee Dipyridamale fnterfere Coronary autoregulation ee ‘t 4 a e Votodlaton ouurs In ischemic Kno tsebem ‘ e AtLat 50 blood move awouy trom Offer, “Coronary Stee! Syndrome” Coss ) Dipyidamok withdrawn due fo CSS Fa. angina . J Mifevatc "blood flow to iSchensc areas only soit intagere % autoregulation © 988 SSEq: if ic gi Ticloptdine cade Clopidogee! AIL ake. Prodiugs $0 they have to be Prasugrel- Gotivated by en2yme Of dug énteract, thee oFdecreate 50 cevetop Th A cagrelor { wot prodrugs , rectly active a. Cangrelor Orag interacton decreased - hav tobe (3) Platelets hove @ Gply fi, , the Blocked Hy , ter, Go Telde ~ |. Abciximab gavore" 1 a. Epri gibatide 3+ Tivogiban cv ets: Prophylaxts. Antiplatelets: an are Used fo cotdiovar cular events Sle + Bleeating (Bx MRR RR ER NR BRN Rm ‘ lasts - Aeticonguiets ding on route * Depending , . | Pasenterat Oral € \ Unpractonated _ iqhibit Ko W Hy € Heparin € tot Hepat move Selectively 3. Low Motecway c iohibit Xa than Li, € 3 Syphetic Penta saccharide: only inhibit to Ke 5 don't inhibit He4 vw ee unfractionated Heparin (vFY) wae @ e ° - ! a e wet a psa dole” e AT-Roli thrombi ° Sa Tepaxtoate - e " Factor fig - activated Prethrorbie e Protamine sulfate e © e 1 M0-Ar Binding to Ank Thrombio fi Bind to AT- 3 ia a @e Lv J @ FH gi ¥,=f - ° e wock Fa = Be tm Block ¥ (Fa? Ta) e. & Rout. 2 @ . ao se sfc e +2\v a ee t Greater sfc Bioovafiatit ee cant give I/v ee & PPB: T Plasma Hssue protefos (PrP) No binding PTP e 6 Biodéng ee 4 Antcoagquiant Less predictable & more ct Ppredictar th ef epect less Consistent because A consistent bee ee Pre @ no PTP @ € 5. monitor Monitorio; / ee Q.PTT (ontougulant yet 3g Rguiony. eae ee achived oh nt) wg @ ; a © & Placenta Don't Cross. because Cross plaantal Cross ‘te e e bind to Plasma protelns Garvrict ef tn 1% trimester - prefered @e Passntaral Anticoagulant yf choice ee metabolised fa. oa F. Plasma raat . ° Hepatrase sptabolised Hepasinae een: ! lesser- Sle 1 Bleeding : 2 Osteoporosis 3: Hypocalamia fF : “ antidote gy Heparto:- Protamine sulfate, uo antdot. fot Lowe Preferred than UFH except LMWH on fat utes Except | 1S qetenester of Pregnancy 2 Renal Failure. Synthette Pentasoeshasie: 1. Fondapaxtoux: a. Tdtrapasfioux- 3. Tdva biotapavinux Oral Anticoagulacts Bw a a a a a 2 Rot far in:- Tahibig vit kK epoxide reductase NKoR — mena — Protein Lu vee K epenide reduechase high incidence | Polymonphosins ° Wild form ¢ many alele Form Nm mm i v Each give diff ‘soxmayes hich aue ot Sata |v'~ o | Effect y WOrfas.tn depends on Vit kK eponide veductase VKOR4 Isoeayin ee ee depends on Pharmacogenetics - °e e e Before starting Wargatln, Screening FOL VKOR, Polymorphism | Tet e e Ra e “5 A 0 sexeening, staxt dase: 2-lomglday oy not, * dose eé : DR © © monitor PTE INR maintain bho 2-3 to Know the ofect gy di ee Ine . 3° as Hox gaxio, e Neo e® ot Sut 62. Dose:- 2-lornglday. ef $0 T dose Monitor PT € INR 4 wouter INR - 2-3 ee L detec 75 e e ig gen Ce — Carle given to 45* Tefenestor of pregnancy. CAUSE - om! . oe Fetal warparta Syndrome which 1S me Conoenc’s Seyne e y genetic Gaus e dus fo warfattn Use e e Chondiovis Pu e of Nasarin = 14, - 30-Yohrs - (B6hrs) Onset Sdays-- days: warfarin starting dayt cause dermal necrosis gt iohibit Profi ‘C’ W'S’ comse clumal problerAlcohol = > Ethanol 2: Fomepiaot 5" competitive © a Mcobol Athy dee peraie 3) Hemodialysis x @ «@ Icoho | € @ Al at nants vs e Aataldehyde ‘i ° [posrude dahyduoginate <° Autic acid Cocsity eliestnated From beady) €e :thano}- - €@ ms A fe icft Joduiterated “quer Methylaleohol potsoning:- consumptfon tuiert Jodutterated Uyuct @ @ e ‘ € e Tonic. dote ey Methanol 60 -!00 mt € ° «= MS mt kg x60kg € @ = FSme fe € @ Methanol €0e | Mectet dehydrogenan. «° . Formatdehyde fi e J Merja auryrogenase ° Ce bods é Formic octd Caccumatate f0 body not excreted &y dy) e y fe Coube Toxtaty . 6 | e fe & Snowy vision ¢ @ Formic acid Toxicity couse | Retina - Obscure 4 : an? Complete bUndness, € Deposit _ io to Sg. optic newe ¢ a Mettylatcahel Ry. Ethanol —» Satutal Alcohol dehydregenak Ce Tv & NG Tube Poisoning cad sclresg 0 cma @ @ @ @ e @Disuigivarn —> Competitive Inbfbit aldehyde clehydiogenate » 5 But autoldehyde deposit ~> cause anpleatant Yeaction. Rio “Alcohol withdrawal Ateoho! withdronocal™ VaR > yt Bt > Aeutes- 1 BzDS + Eq:-b Chlordiazepoviae Cdoc) 2. Diazepam oe eat ed Antlevaving agents. Ceeduce cvautag) Detereens- eter pom Disuigivany — atcchor Acomprosale CCCCHOCHCOOCHOCOO OOS SSSSORFFH MORO BANE Metronidazole Topiramate Nitvafeaole 0 ndansetron @ ) 2 Naltrexone e ° F tuoxeténe ef e® Disulfiram Uke : 1: metronidazole ee Reactions a Nitvafezole 6 ee Aotigefaure Drags 86 Clamity bared on Mechanism: @ ef T- Na Channel Stockade: hd / ee a T type Ca Channel Blockade se GB. Drugs that act vfa GABA f Transmission © 3 Ww Mis cnineousI Phenytofa - Phospherytoin 2. Covbamazepine ongcatbomoupine 3 Valproate 4- Lamotrigine 5: Toptramate 6. Locosamide F Rupinamtde used to Lenox Gathaut Syndrome. (C6) Most vecently approved fot L@s is Clobazamn (820's) Phengtoi >)" Block Na Channels: Ctractvated Stat.) > Not allow drug 40 become aad ORD mm mM mm mm ow > Protong ryractory state y Tissue > cant tigger Seizure + omnet og next ap fs delayed. é € Phosmaco kinetics: Ik oral & Ziv € 2. High PPB tt é| 3. metaboiiaed by CYP 2c@/q in Liver : 4. Phenytoin is an enzyme toducer comps C S> Noxkow Thesapeutic fodex Caw antisetaeas) « &- Therapeutic -. 19 - 20 Mg lme. - eect in platma & vangeF- When phenytoin Conc? in plosma goes ? Vopglrat tt follow 5L zero ord Kinetics - Though it is Reto ovo kinetic, Toxteity do Occur: Toxicity - >ao ng hme Uset:- + Genexalfsed “Tonic clonic Sefaures 2. Focal Sefaure. Cpartial sefaure) ( Origin From one Focus) 3- Status epiupticus.- Fot this > Fosphenytotn - only by Thurow 4 Antt arytimics Celass Tp) SE - Toxic doses Cmainhy newrolo; Therapeutic does ‘ {stu ances Hivsutt | Behavioural olistus bans * Hyperplasta oy gums 2: Cerebellar Signs> dtyasiinta, ataxia Hyperglycemia 3: Drowsiness ‘Hyper sensitivity 4 E pigastic palo Tevatogenteity- Fetal Hydantoin Sidiome §. & an te ap Ostomalacta 6. Hatlucination Megalobtastic anemia. Heparin Stewidt Phenytoin—> Osteomalacia . j OsteoporosisBinds to inactwates Wa counners Y Prlongs Kegracrry PewE S Phavmacokinetics:- > Oval > metoboaed by CYP3Ay 4 « é > Hsuf Enayme Taducer. — Autotnduction & Metabale > 10-,N- epoxide is a metabolit of CBZ Uses |: Focal Sefaures 2 “Neuralgia Trigeminal, glossopharyngeal) 3 Good altemative to Lithtum in Bipolar disorder Cmood stabivaer) 4. ile ayAcute - >7Kgiml SJE s-1- Neuxotoxic > arAcul gl es Index Thevapartic Tange = 6-12 palm Coxtamesipine >> Phenyboin 9 overdose wer Qemoved by Hemodialysis By Hemodialysis, Molaro Dero order kinekes Rashes & photosensitivity « Hypersensitivity — TEN, Steuen-Tohnson Syodtome Reactions Cause agranulocytosis > Aplaste Anenta . Anti diuresis ) *5- Ho wtenfion (‘Syndrome a Toapprepriale 6- Alt Qntepiuptice ate Teratogenic Doc io status epiupHas is Lorazepam - Ze] (ER ER ER RRR NNN RN RRA NSOOO COCO OCOE OE ODREODODEE e@e000 Oxcaxbazepine BS aes 7 Tt has lesser S/E than Carbamazepine. > Efficacy % Ooxcarbarpin & Carbamarepine is Same. + > 80 “Oxcarbazepine” is used, where C82 (Ss USed. fa all- > Doe For Trigeminal Neuralgia. + Beller for Focal Seiaures: Valproate Sodium Bee ae au > Standard for all ype % Seiauvea because tt has No® , 1 tye©, Gaga enchanament — mechan/sins + Predominant: Phoxmacokineties:- I Oval: / 2: Metabolised by glucorinide Conjugation 3 Valpwat itselg is CYP enzyme tohibitor- USS: | All Kindle, Of Seizures. Doc - Alt Sefaures except + Focal Seizures Stn atypicat also 2 Typical Absence Seinimes 2: Mood stabilizer - Gipday disorder. 3. Migraine prophylaxis: SJE bk GT sympims. STAIN STATIONERY 2+ Neurotoxicity GAUTAM NAGAR 3: Hepatotexici ty, ogesuea say ») 981198 2449 - & Rashes 5. Alopecta-v y , «@ Divalpsoex - 4@e@ «@ + SE less than valproate - ¢e > Efficacy much less than Valproal € : ‘ e Lamatrigine fe €@e M-0-At- | Na Channel blocker D ¢@ 2. May act ot Glutamali release Johibit- Erhasucnide Cot ong gC San faky a) Aryptcal 8S —> Nalproate - ¢ @ . e 5) Doc Fo AS—> Ethosuximide Chet rot Avoitable India, soure © @ vaipreate) ce ie Indi y) Doc fe As in India Valproale - e « @ e e ®@eee0GoedOeeaeooedvod @ ®F°S2880 N20 000: © OB RSO*KM SSS eae ABA cu BG Drugs act on GABA mf PGABAD oH x : s--Coost att 00 ‘odirect “Gaga mimeTics:.-Coont act on @) Gar-4 - Gaga | Progabide- metatotiae GAGA in synapse & nero v ~ Prodwug- Geen eee ide medatoliae Ge foedacts teynay . MG - ie Tiagabi 2 ABATRIN- block GABA Trancaminase Tlagebins Gren Transominase Uuhich metabouse Gaga) & + Gaga. ¥ S Rencnee = Drug fot Togantile spasm, couse hperpaata ooh ae: 2-CL foplux 3 Pen ev chan 3: Tiagabing t+ Block veuptake 4 Gaga Bock Gari. & TGasa- Borbiturotis Y B2D's:- au directly acting 00 Gaca &) & on oF Channel duuetop 1 act on GABA but they act Predominant in = Gabapentin { © => Pregobatio Uses 4-7 most Effective drugs fo Nuwopathie pain. eT Type Ca Channel ds Bipoiax disorder 3> Migraine Prophylaxis 4 % guiedat Tenduney Ta Tips 22 Ceovel Sten 1 Ethosuximide. . a. ZoNSamide . —Sulfonamide derivate - long Ty, bo 65hrs 2 - Mainly fA Refractory Seize, SJE~ Cou Renal storeseo £ ew am 4. Pregobadin a= . ¢ ANKE pilgica Cause Renal Stones :- |: Topiramale Crete preferable) 4.20 Zonisamide Migraine Prophylaxis. Propronotol- < Tea CAamitypt ytine) Valproate - T- Type Ca. Channe! Blockers Topiramate - Gabapentin Pregabalin Flunariaine Mmethy sergide - cyprohepticine Mitscellanous - - Felbamate:- t+o-a:- Nimpa @ antagonist For Staves SJE 1 Aplastic anemia: } an verge tattbcrousal die a. Hepatotoxictty to Sle- + Levetivactam.:- m-0.9:- unknown’: = ack by binding to protein SV2A in al Use tk very good add-on dug S/E # Ataxia 2. Diplepta NN PR RR RR RR mm aP2822 009 0 BH Epiupoy Lo Pregnane + AN ontiseFzures axe Tevatogunedity. Leatt Teratogente which ic uted - Phenobarbitone ... sagt fn Pregoan Ll v Lesserigieany OO 19 PND v break Hrough Sdaures more danger to Fh Now main aim to prevent break Through Siaure » & Use more ypicacy drug current guideltors :- drug , continue Same dry 1 dh a Fema ts on ant convulsan! on pregnancy. 2: of 0 using aneonvurcant arag, give fhe drug cahichon the type qf Siauxe— Uae that drug Valproat .~ Doc upto 00 mgldog is Saye © Yespect to Teratogenecity. 3- monitor Youttnely- 4G. wo single dug 4 choice Anticonvulsants ted in pregna Phenobarbitone Cause > | Sedation } jin Fetus: 2. Repicatory Suppression Today "CBZ - Safest, drug fot Seinure To Pregnancy > Phenoboutitone - Least Texatogenectty BND Doe. in pregnancy fe Seirus:1 Mu ® 2- kappa.© ~ 3- Delta ® Codfene fsdrug et Tras 4 Sigma @ + action on Oppi d agotnist on Mo ® + physical peter loc :+ Ew nucleus . org - 2-ens Miosis. © cntrally mediated action se or Constipation Anatgesta. Resptratosy Suppression « ‘ é é é 4 4 é é « € € € é € E uphowta Sedation. é é a. Kappa @ !- All other actors au Same Uke MAS except: : Dysplasia fo place Euphowia, CPMCARDS) z = eed gee € + Pethilnemepeine ¢ metabolised y € major pathway nin Pathway C ane Nox pethidine -» ability to aa i. J . eliminated by Widrey.COCOKBOHOHHHOAOHGHODOHHO8288OHSH8O8 G CeCHCCCHHLOALODFOOROOHOOO® Nopethidine Cause Sefaure nk Renal Failure . 80 eI. 5L 2. MAO Inkibitors.+ pethidine v = gisk a T Sefauxes. Methadone - > tong acting Mu ® agonist kw detected [A plasma within Somin > Rapidly absorbed from GIT apter oral administration - > Relieve Chronic pain Ccancn pain) € onset F analgesic action by pasenteral + [o-20mia > Analgesic: oral. - 30-6omin > One hue to Opioid withdrawal Fentanyl I+ Short acting drug TH, 3 Dory cave Surgery - analgesia. — Fentany! -w : SuFentany!-K8l short acting . Alfentanyl-ta| Remi fentanyl “2 20min Drugs for opiotd withdraw! piore + but abuse. > use opioid © agonist » Methadone — produce opioid ee 4 Replacement Therapy, > Use pastal agonist. 1: But orphanol 2. Buprenorphine 4 o> Antagonist Use :- Nalt woxere - ~> Le acety! alpha methodo! CLAAm)Naloxone - ured tn Opioid poisoning. Bat dwg fot detoxification & Prevent relapse is Methadone. but gien Und Superdsion admit in hospitar) so given Naltvoxene fn home '9 0p vegimine sp drugs which cause detoxigication but not Rerapse Prevention: |: Clonidine Antips chotics Mon: Blockade 4 Dz Receptors AM 2 PN EN NN BR A RR ER Rom Taeica! aryptcat 0, @® Predominant. predominant ad other than Neurolepties - 0,@2 . . > Algo Block O,RS i “ ati, Ronly He Symptoms Adv:- Both ve & -ve Symptoms 4 % Schinophrenfo Schfaophventa KX also Cognitive € Smpairement C » x 2. Effective to Resistant Schinophratac cho. du to abt "3. Also wiefus to P8Y . * cous Uke Bipolar Asorda | Organic. Brain aisorde. q x substance oi , 4. mood gtabitines ff Oknzapihe %@eeeeoeaoeeeaeaone ood SFP CHCOHRHE OBOE @eo00e@ e@ee08 Amphetamines abuse mimic paranoid Schizophrenia . ot Typical Atypical 5+ Extra pyramidal Symptoms ers) Hyper prolactinemfa. D, © — 7 Prolactin Lesser, EPs & Nypexprolactinenia.. More tnefdance - eae Drugs owoilable fo /m Depot:- , Haloperidol > Typtent seaolupte cen eo. ‘ ste IT Fluphenoine Uses of TIM depak.. f Pt InCompliance. 2. Oral Toute is not available Sle .of Aotipsy chotfes :- SE eee Tyee. Atypical i bo sje mainly Neurological mainly metabolic L EPs ' Hyperglycemia. 2. Hypexprolactionnia 2. Hyperlipidemia 3: Sedatfon, 3. wtegoto. cecum > Clozapine:- Sedation, COU 5. Set gues 3. Agranulocgtosts - + Zfprastinone. 5 cure Ws tot gain, - AlprastinoneThee aus din t0 0,0 1. Parkinsonian symptoms Ct Ach ‘Leads to this): &* Central anfichoUnergic. A Akathista CSubjective or objective Restiessness)-4 Propronoiol 3 Peri-orat Tremors. Rabeit syodome)- 4: Aout. dystonia > m-Spasm. uiually occur’s caithin 6 mon gfbtoring by 5+ Tardive dyskinea> Swotuntary movements. beyond Enon y Starting Ry G. Neurolipiicma tignant Syndrome Cleatt common but most fatal) cums) ‘ Ryu Ib Decrease the dose @x) Stop the drug. 2: Fo 4+ Paxkinosostan -> Central anticholinergic. a.Nmg —> Bantrolene, Bromocriptine . 3- Akathisia > Propranoiei . New KeMmSyndl : - wOLepeM Synod ome “1 Aatipsychotice Ctypteal: > Atypical) 2. Metoclopiramide . 3> Domperidone has Very negugable ect 4 Crss San. DORN RR RRR RR Rem RD n>.CelCCOTAE OOOH ODO AEODD0E8 ee Mood disordes 59 4. Mania. 2. Depression C Endogenous = Insight © — Pure depression. 3. Bipolar disorder . 44 Rapid cyclers (transition fs very vapid) Drugs Foe potar, Disorder. Cees Ww Litiiur mon: J Cellular metabolism Cask, 3p, PiP ete) overalt depressant Mechanism on CNS- Usa 1 Acute Episode @ Mania. 2. Cipoiar disorder. Doe ~ Lithium Rapid cytes - Doe - Valproate - 3+ Cluster headache - 4 Felty syndrome - Li asvatis neutrophil count - Plasma levels :- Maintanenae:- 0°6-1-0 meq/L- Acute = -0— FS meq|L- Toxic = > ameq/e > Hemodialysis is exfective 4 Ui lds > 4 meg|e2 Tremors (Fine) < sje 3 Hypothyretatises 4. eater toss Gh) Polyurea — Ofabetes Insipidus: Doc amiloride 5: Texatogenecity - Ebstetns anomaly. Atgpical Olanzepine fo Bipolar Aaorder din Pregn dings Reaperidone {ane ns Ee Trteqetic Antic OS Mo-A‘- Neuvotransmittor Reuptake blocks NA, S-HT, Copamine al Nesrotrangmiliers ee Mean Nturotransmitor fs F—HT Serotonin. a i a => SSRIS Sdectively tahibit 5-H: VLR ‘ . u durertion tuoxedine Cactes “tLongest act & 1. Fluoxefigg —> Norfluoxetine sangat e ye 4 2+ Fluvoxamine. anand yPIo—S ¢ 3. Poxoxetine - é | U> Gextra Line ; S + Citalopram ‘ 6: ES citalopram (Es- anon) ‘ : ¢ Uses to FAN forms depresion seartte a. Aout. atack we Disorduts Cphobio. , panic diserdue « “ ssais “9 ezo'sSOCCOCFOCOCAOROOH2R00 SJE + G-T Symptoms Nausea. 54 Diaxthea. - 2- Sexual dysfunction 3. Paradoxical anxiety. 4+ t suteidal Tendency. Flumazeni| : 1-820 antagonist: B- carbene Lome Zo Mond. Act on GAGA 4 @,> S20 St. 3. Tv given i 4° Ty Ahr. &%. Duration- 30-bomin. CHo min) Wst=6 B27 overdose | poisoning. Sie Rormettenn:- Cause Sefaures. (where: B20'5 v Seizures) Ramelteon :- 1 Synthetfe melatonin analogue. a het on MLT-1 , mT-2 melatonin @ agonist 3 Oral bioovatlability <2‘ Gq TY, & ahys x, 5S: Pegs 80+. 6 + metaboliad by CyP - 450 eniymes - FA used for deug Ry tn fosomnia BM negligab te addiction Potential1 Anti actertal Digs: 4 Costegentes TL. Drugs that block Cell wall synthesis. GZ Orage that block BD Orgs that {Drugs that Tnterfere % Folate metabo! protein synthesis Inhibit Ona gyrase - tism* k]a Antimetobolites Inhibitors: Cantioactefal cell walt) + Cell 1° Syothests I. Celt watt “Sy reauneees ' Depending upon Structure divided Gy Glycopepdes - strackus - Cy Brlactams struct 1 Penciiting 2+ Cophalosporins 1 Vancomycto © a. Ticoplanin 3: Caxbapenams- 4+ Monobactams Grom +ve => B- lactams. hax N-acetyl Glucosamine (8AG) a peas N- acefy! muramic acid ama) —l-va—-O- a ayn KT o-—m-a oma ow Trangpeptidase Cross Unks Foard in Penditin, ° Transpeptidase u no sts Unkng an A a a a a a a a a a a a Ne mm SOHOHCHHOSCHOHHEOSHOHHEHHOTTHOHVOHOHHOOHLOHOXVOCR®Seo; ne 2p bind, - | e Penclilin btod to penefiln wutng Proteins Y inhibit Cll wail LO ° Syotheus ee An B- lactams bind to PLP XK Inhibit cel taal Sypthat. . ee Camox, pipercinin et) @ ae Penetiins Cen) 6 @ e A Natural Pencillin :- From Fungus Peneillia notatum. @ ee fF Pencittte G. (Pag) | crystalline Penettin | Benay) Po | Aqueous Pa. ee = Acid Labi. ee = Very Short Octing drug + Short TH, @e . ° e To tnereate duration Pencillin Conjugate ¢ @ e 1 Procaine +Pn —> Procaine Po 6 > Lecat-Aneatiasin e 2. Benaathine +P —> Benzathine Po longest acti ee BS Repository Po Preperation :- Procaine Po ee due 40 long dusabonsy Sennatthine Ps e . act” e °? B Semisyntnetic. Pa t- ef T. Acid Labile - Aciot Rexistant Po, ef ere he _= Py V - Phenoxy methy! Pr ee ° yeti 1 orally ache: became ee 0 - Oxacillin acld Resistant. | ee D - Ocloxacitin K - cloxacitiia A - Ampictiin A - Amoxicillin eog eS e@methicillin — Become resistant because altered Fencilin Binding Proktn, @ Naf Cittin @) Cloxacittio @ Oxacitin S) Dicloxacitin or a a a {Pn G has Marrow Spectrum act” only effective Gram $6 K Some Gram -ve: 0 developed which act on Gram -ve also They oe he Extended Spectrum Py: i : « J. Amoxi Moxi dition to Ya Aminopenetions aut eyjective against Pieudoneg 2+ Ampiattin € 3 Bcorbenicinin } Carboxy pensillins € 4 Ticarciltio € 5-0 Piperacin Beat Po against Pseudo} . Usiclopenciting - € 6+ AzI0 cillin “ #: Meziocitio ( 4 Useg:- Py G@ Docs (Leptospirosis caused by L herwnagzca. € @) Actinomycosic Cany Hyper € G) Rat bite fever. - caused —» Spiridum minus : —strept bacittus monitinug © Benaattine Pancilin, O0c:- (Syphilis Can) c ot Cf to» Newsosyphiles becaue i toorse ns € sion On pose’ es par Neurologic. Symphoms. € So give Procaine Pa (a) Pa G (> Drophyias tn Basmatic. ae © dus torts Longest a € UY Repeating adminisSle og Pencittins:- . Neusotoxietty. Ait B-lactoms shove 2: Hypersensitivity. Reaction Cevoss allergy) 40 each ober. 3: TJaxtsh-Heviximer Reacton. in Syphilis. ¢ ReactPage: TP! 4 Ampictitin C/z in Infectious Mononucleosis becat tt? oth. Cephalosperins ces) x Gen :- CepLothty, I’ tndicotion:- Cefa Zo Ute Used Fo Prophylaxts of Surgfeal Fo gections - CefaLExtn . Cxqo RA dine GfeDRoxiL. qd : WG? Ce Fac tos: Used: CefaMAndote- matoly for anateobie. fnfecKons. Ce Foxitin: Ce FUR oxime - we gen > Cf TRloxone- Cegta zi dime - used CefoPERa2one any ft Gram ve Tofectons. Cefo TAxime- Cegti zoxtene-Cefptvome: tuted for, Nosocomtal Fnfeettans, I™ Gu Ceptobtpfrole Ceftavoline Frovoln Vactive against Mes also, Ebieninabon:- most @ Pos & Cs eliminated Prom Kidouy unchanged Po Ws wequtre dose reduction tn Renal Failure . Cs which don't require. dote veduttion In Renal Failure XB AR AX M rm Mm Mm Ceftriaxone - | they aut. vot Liminated by kédnuay ,elenineted by optrazone. ober ae Givary excretion é Cepoperamidle - EUtmination tn Kidney 0 Pris & Cs € y i @Tubuler Secretion € OD Glomerular Filtration Probenecid inhibits Po secret 4 plasma levels @ Prrecs € Coxbapenoms. € 4 Tenipenem +> Rove: Tv ¢ 5 metabotiad by Aihydvopeptidase - € TO To preunt metaboliae- ¢ Cflostatin Target & : ‘ > Extendid Spectrum f- lactamase Ese? a « Cleave almost all fB lactoms. ¢ -Imipenem Can! be metabolised by ES8t ‘ - Tmipinen eistant to Eset Za — 3a ESOL tre, + Tmipenem é SSCHOKRHKHSHSHOHSSHHSHOHRHSSOHRHGOROR9HRHDHOOHTHOHOKBRBORECOKCHOHOCOH ROCCO ®S 2909908000004 e000 ©0008 ef e¢ unjeaners Sn mperenae be Mexo penam, Dovi penam Extapenam Fox0 peram fine eota D-alany! - O- alanine inhibit DVencomycto:- mows 8- Cel wall synthesis . Pharmacokinetic: - Orally - 90t absorbed - -a\v - atoays - Ty, - Ghys. Qld = Dose S00mg ain. ~ Eliminated unchanged in kidney. So in Renal Fe dose has to be vedueed- SJE = |. maculopapulax Rashes —M-c. 2. Red Mann Syndrome: because histamine release beca Vancomycin is baste dng. | 3. Nepbrotoxic, 4 Ototoxic User - 1 MRSA Infeetfon. Doc — Vancomycin 2. Drug tnduceel cout's Cpeudomembrancus coe aA n 9 ovat-tut © Doc — metronidazole Vandomyeio bat 004° topteat\- Vancomycin. a a a a as 2- Tefcoplacin. Resexved fo. Vanco ® 3- Linezoutd: _7t 4- Quinopeistto | Dalfepristfa.—> Cstreptogramins) 5- Daptomnycion. > Reserved fot silo & Soft HSsue Ingections. 6. SJE Rhabdlomyotisis - 6. Muptvoctn :-» Doc: Exradfeat.- natal carters | (staph oman) Rout. + Toptcal 2% Ofnt- F- Cotrimoxazole %- Ctprofloxactn ; . € , => Neomycio io hepatic enaphalopathy = Oral Route but ad Zppha ¢ € 2 4 > Conjaness of Vancomycin:- ‘ |. Telavancin @| 2. Delba vanetn : 3. Ovita miifefn € ¢ ¢ € qb> e | ev 96 Drugs that block Proteto Synthesis | gs Ok See - ee oe ee @ e & Start codon - AUG, eo © me tefonine ee ee fe @ a e dove by pepldyltransgerae (Ribosomal £09 not proteln) e 6 O©CHoramphenicor @ a ee Txansiocafon Cmovenent % Ribosome) oe ‘© From a9 'P site macrolides ee oe EQniay oe 6 ar r Cindomyeto e ae a Uocomycin, oe? aire ry oa, @ @& Protein Synthesis Tohibitors:— ee 2 ee 4 Peciinogly co sidis :- 1. © Petysome. Formation Hon . . 6 2. Oisaggregatfon 4 already form Polysomes ®@ 3. misreading gy mRNA Code- se 4 Freeaing Y 'niHatlon a protein synthesis: of of SD Tetroyctina + te Binding Y AA to ‘A’ Site block e6 = Chiovamphene cot Se ee D> Macrotides = exhibit Cross resistant clindomyen & Lintomyesn, e Lindomycin & Lincemyein e because oy Same binding Stebt ae Tetracycline Cte) — very high “toetolence 4 s]e so aow-a- days cot used. - Conjearers:- > Pony cycine > Mino cycling > Deme cio tyctine hadmacoine tics : P asokinetics Te accumulat: i ReHeulo endothelial gwetaboute axe cxorcted metatoiiaad 19 Uver toy kidoey Lives @ Renal Failure e € € € € « @ « calls: é é é dose eduction 70 ¢ « ¢ € > Require curds cheep Doxyeyoline > metaboiud io Uver doxyeqeie Qliminated to Bile o honatis otto cme gJert GI 8 : ait Bis phorP I yptoms iw, Esophagitis ora verte on Esophageal weers P 2: Deposited to Skin - photosensiization, hyperpigmentation & Nail — nail pigmentation . 24 . 3: Nephrotaxfcfty — Al Tels cause except Doxycycline ¢ 4 Demeclocyctine — cause DIoripidus ¢ = "80 one oy dwg tn STAD! ¢ r ¢ : poc - Vaptons Outdatid Te taken, Come — Fonceni!s Sy! ,wv ind 5 ty htt e® SJe aq TeS io childyen:- oe é ee 1) P Ter so % Cause Pseudotumor Covebst 2 Taken highdose got ee 'S Me: cause Tolopatt e e 2 -Grawth Retardation & duntal abnormalities .Cdincobration, staining, . e matformation ) @ 3) Teratogenecity. e & ee Te's C/rs & Pregoancy. ; 6 2. Childven -< Byrs a e@ Uses: - @ Md “ af Oonyoyeline:- oc for. 1 Grucenosts. < Doxy cyclin + Rifampicin e e€ aqrégante 2 Cholevo.- 4 WmTe AS 3. Ricketistal tngection.- Epidemicx Endunfe Typbus Todian Tick typhus RMSF- 4 Lymes aTseare - 6: aorgodofess 5+ Relapsing Fever. @-Recureotis 6 Leptosptrosis <— For Prophylaxis: Pr G <= Doc: > Glycy! cations: Meo class a aotimiBrobial dug. - Derivatives % Tels, Tigeycline. (mo-a w% To Te's) = unctu waluation oY Reristant infections Ga Man, Vet Tain STATIOVERY GAURAN rAGAR O46 5464324 7 © 9FN98 2444—eIEeooorr aambits peftidy! tBansferase eoayme M0-A Photmavokinetiar - Given by any out. ste also- - metabolind by Glucorinidation — vat proat Use: Restvicted Fol some only. duu to t S/E- acteval meningitis: 2. Typhoid Fever. 3- Oculax Chiamydot Ingections - ee FPS Crrachoma, Inclusion conjuncsivitis > SJE 2-1- Mydlosuppression - 2. more Toltesynerate. reactions may occur af any dose. & Grey Baby Syodtome: => Macrolides:- Aaa 0" “Gohibiion Translocation. Doc For Toxoplasmosis in Pregoany (BR RR ON ERR NR eg: Spromye? te Prevent Transplatntal Transmission SOCS9HSHHOHSHSHOHSHSOSTHHHHOHHGDOHKFHOHOHRCHHHBHOTSA 2 Claxithromycia :- Doe — Atypical mycobacterial infections aM 3 Azithromyco t= Doc - whooping cough — @. pertussis = Atypreal Preumorta, ~ me=Mycoptono® oath asec do! is patos rt Foe Hs Pe 50 kantant lo Gn can Takao & ~ chlamydia Trachomatis Tras! AB DAC . ~ Chonewid CH: aueryi)020680 @4 ©0000 00808000000 TOHCOOOCHOHOOOCOS COSCSCCOCOOHAXMLHMEO OOS ef = Donovanosis Ceaused by Calmuyto bacterium intractielan) LF Specteic Indications For Erythromycin:- a acer et wn Gr gt is a motilio © agonist: > 7 @ menUty. Za > GIT > as Prokinetic Rheumatic carditis, (Re: > of pt. Po allergic pt- Prophylaxis % 5 Exytriomycin is 0c. > Prophylaxis Fo Re ,Hpt- allergic 40 PaG, Ougs used a6 Ce Se ‘ > \ Sulgtzoxazole Csulphonamide) > 2 Aztreonam Cmonobactam) “Kk All p-lactam’s Show Cross allergy except: Aztreon0rm > Exythromycin ~ doc SJE q Macrolices:- 0) GI symptoms: b) Hepatotoxicity. ont ; ) cause ©) Ototoricity. < mnoeycltn (Po v D> Reversible heating loss. Cmanigettot?) Clarittwomyc? Aerino glycoside, cay Mor-a:- Freeze taitiations gy Protein Simihesis Phatmacotinehcs not given orally, hot absorbable because polar Pokenteral Route only 4 don't penctreti BBq 2 S07t Can be ted in * * nae Bacterial meningitis. ¢AG's dose veducton fo nal Failure. ® é =D USES! | Very effective 9 Bacterial Meningitis € Gentamycfo (aes) é Amprditin (@road spednun! ‘#Bloctem) é € é act". Topical in hepatic soesphelr ay 2 SABE @> Empivical Therapy Start © 3: now-a-days very effective 1 “Tuberculosis. 4 Wleomyorn > Route -oval , 5 Agfective tm Aetoble organisms, Inepective fe anartobe, ‘ € SIE | obotoxicity ¢ 2+ Newo muscular blockade, ‘ 3- wephrotoieity € € G. Tevotogenecity © oaly in coed a t " DONA Gyrase Enhibitors. nhibit own gyrase - € Quinctones Fluoroquinolones € pe omer oR ; only Grom tye — Topoisomerase N enzyme ” baw «| only. Grame -ve — Gyrase « e Oe not given GH) | > - Gyvate. € Phavmaco kinetia = Oval, T[v route, € Flucroguinolones voukes. ¢ ¢ Fe's (Levortox) ~ Oral Bioawallability - ~ 100'/. ¢ C 2O00HO0HL8OHHHHHHHHHHHHHHGHHHHHR9HVROO8Ee|% FOS TY 66 e\e 1 Ciprofloxacin U hrs a : id ee 2. Noxfloxa cin Shrs ~ : e 3 Ofloxacdo 6hes e e 4 Levo flovacin ef come pan f hrs @ 6 Gatifloxacin ee e Ss Pepoxacin lolns e e e 6. Moxrgloradin (Lbs e 4 a) 4+. Spargtoxaca dobes —9 Longest Reting.. e ° Uses:-1- OTL @ © 4 ras. Ciplox -72 Tinidaaol . ° sy. {plox - 12 Tinidaaole - © © > Gactertal dfowhea H dysey-» Cipln- TZ Tens e ° Gacteiat Proter0al @ © > 0, Coftox - osnidazole> e : e e 3: Typhotd Fever. doe - Ciprofloxacin. ef ee 4 Resp. Tract Ingectiong 5+ Now-a-d ctive 10 TE C50 Fe uRTI-> Fas ee sa bbe Lare 9 macrolide we ee seca Ray ge vat we we Fas Ce SJE:- | GT Symptoms - Nausea, Vomiting + fd URI 2. Headache. 3: Dizaseess. 4- Rashes 5. Photosensitizatfon- 5 6 Tendinitis y Tendon Rupture - 4 Artheal gia SParfioxacin 8 ate Protonation < aeurenrerinaes eee © Fas tusrios 7 WSK nemotoxicty: © Clprofioxactny ,Jobibit — Theepryllin metobolism. +9 couse death } y Thuophyttin gets ccunulabd & become toxfe- Exytoromy cin becouse Y Theophyli'n Toxicity —> Resp: Suppress”: onus, ote s interfese @ Polat metabolism - prerdine + PAGA » Sulfonamides, \ pthydropteroats svethase OM. Dapsont: . ones) thydvopterore add Lothydio poate Synthate @ . eee Bemethoherdte Canticancer) Dihydo Folic acid « 1 Tatmethopssey [other folate Reductase ©)X 2, pyaimethamine Crue) TetrahydwoFolic acid. (donate 4 Carbon to other) Cotimoxozole:- os SMP - EMx > Cobtmoxazole — exhibits Sequential block. Cee tabo(l + 5) —ain Maman C1220) + DUPS . py 2. DHFR. uses 9 UTZ 2) prostatitis: € ‘Teimethepvin monly accumulates fm Prostale 3) Boctefa dtareheal dysesty: u) Rep: Tract ‘Ingectons. . Actinomyers —Doc- Png. 5 3 00c in 9 Nocar diosis 2) Preumoogtts Taxowiii Preumonia, chine, 7 ARR ARAR RR mm aa mm amma mm aNSle :- becouse 4 Sulfonamide Component- bt C - ceystatiusia, A - Acute Remoly#e reacton. R - Rashes P - Photosensitivity. H - Hypersensitivity Reaction (TEN, StevenTohibo Syndrome) E — Erithema muttifonne k - PI A Kumicteus _ dfsplace biltrubin from plasma binding site. sateen bilirubin, un con)-Bilruti-9axal gangka ‘Al bumio, * deposition 4 16 Kernteterus ay ‘ Bactertoctda eetonosiok > All cell wall Synthese Inhibitors = All protefn gynttasis Inhibitors > ONA gyrase Iohibitors exapt AGS : A Ankimetobolt > AG's + beeen they act bepete etd oboliter except Cotsmoxiaole - Protein Syntheris Inhibition cloaca apitntembtol > Cobimorizole —> eahibie, synergism S + wm Sulproethown, 7 SH Combine (sa) statin # become cidal wp Drugs bind f9! Jos —> Te's Streptomycin a Interface —5 All other Aa's 3 50's —> Rest au4: Cone? dapendant EFect?, Core? Effect drug T by 4% Cone” above MIC (Eon) pie act on micreyal Eger oeug dupends 09 Cone” 2. Time dant Effect + (TPE? Tae Seenees Set mame. sa.@ Eon * Time above MIC - ae % duration ated E00 dapend upon Time above mic Mier idles cone” of dug vqaiade im platma fa diug wD act. ¢ Cpe Toe ‘ € 3 Cone > MIC > Time > Mie é eget Ac's grt B-lactams é he’s LVancomyein € 3 Azithromycin : we (OE of lange domes at oncet Ue Gun fo Sean doses move frequently} ‘4 S day) © eae vided doses (3-4 times. a day, € a j= 300-4000 altemative 4g Siegle dose - on 7 3 « Tos] 910. > I better than ‘Soom € qe on € gonorthea ¢ Levogtoxacin — Ta ~ Bhs: C = Soomg oD ¢ because cone dapendaat- Pst antibiate deprnint 2 Ciprosiox — 250-750 mg Bp SOOOHRHHHHHSOHHHHHSHHGBHHHHHHHHHOHH8HH88OGentamyetn - of give large dose Genta mycin ~ us Tonuty occurs so dose Clee 22O2ER00 0% Fs amg)kg Tos NOW :- OD-> ‘ontcity > 4. fu gee aividid doses > occuratation ccans canton So, gen 00> &mq [kg Jo. make, Peak means act on very large o- ie peer Y wicmorgonion oe ak persiste, even 'f Cone” 7 pect below Mic Om Same mieroarganin Poskacttiotc. efgects- (me) Perferonc o efgect oY Crug remodin Same - ig cone? is below Mic => CDE hove Prolonged PAE TDE howe negligable PAE ame oe epee ere eon Effect depends upon Time df Conc atove MIC 30 they Show Prtonged PAE 6 gr Clodamydin Cnrhe get) Exytnomyein Dwg Resistance -coused by > may not enter cell ee ao AG's aneorobi' 2) W penetration drug ato Gall GAGS A> © 3) Dwg enter into Ga but throws out af Gt FS Active qyplux by P-gtywpmieins (Pay) eye CI on at Surface ") mcmorganimn Cuate ensyme & cave ding ys f- (B- Satta me 2) Alteration Im Taiget SHE ce methicitin Cattert® mn pa tsttviena i Ampligication y Target gener te iD rola Seduclae — 3. & some 7 excessive production Y enaymeys ef et Cancer. Is whch jactvala drug. Anti Tuber culas Drags : Classified into z* class 4 class. => slow > Fast R igampicin me x, rug 1 Oe Z *pyrarinamide > Slow > Best dug fa. * Slow, NB ee Ethambuto! 5 Fast Streptomycin Tsoniorid act on Raglaly multiplying bacteria (ma) Roth on Rapid & Slow € predowinant Ro ae eB a € « € « 4 4 ¢ q « H Teontazid —? Fast Gest dnug Fastne é € € < € € € @ « é we F penctrat, “Caseous necrosis € y become Sudden grow € Ripampictn - best Aug = , ¢ de Preent in centre @ Ceseous neaosis 2+ Fost growing Mycobacteia B. Slow growing MYCobacteNs ©SOHO OCHOHHOHSHHHOSOHHOHOHHOOHOHOKRGEOL OO Coeeeereeroeneneeg0en eg I" Une drugs M0-A' act by Inhibtting mycolc acid syothes Cal H& Zz? E + act by Ttolibiting Rrabino galactan synthesis Coat w Sv “Iobibit q 1 Bactetostatic 1° a wal Synth, inhibitors) 1a Syathe tabi birees Inkibit RNA polymerase —> © Transcription so it becom 7 © protein synthesis Yeitiation @ Translation — © prtdo synthesis - Une anf TB drug > Ethambutol- Remaining ait 52 Une are States , a. Nok given oralty — Streptomycin & AGS4 polor compound pare 3 Ooty 1st Une _ deug given fn Full dose et iy Renal Failure -Nodase Rec Rifamptco- rt -b shows Predominant bivary exexction- @ S[Ex Hiv} peripheral Neuropathy. + tT Indian poputat? show ream 2 Be debieeney Stoo acetylation so fost a fay Bg Peps tong doy move chance 4 Pat | aurie*c| hmmm 8: toomglday pa - Pyridoyines L- » Pgs oxinee dopa Neurotoric, not used because Hepatotoxic Be W's Ldgpacie : et SLE -Like syndrore- 2 pyrtdanine (eg) # z2. Suddin Hgbtening in abdomen Chet & Inqpiury Ty vreue Acute Chest discomfart - 3 Acute abdomina! discomgnt Cabd- distent®) 4 Hepactotoxie paca hoe 5. Cause Hemolysis (@8e—> proteins —> &- Ovange diacoloration % VSne Pt- tncompliance. So pr sl Sle Z + b Hepatotoxic <(Host) 2. Hyperunteemfa.- 3+ arthralgia. Sle Eb mafole Torte to Opie werve # Refina 1. Opie netic ushich J vision 9 RIG ny Cause 2. Red- green color bUndness Retina, Blue | gre color bundness - Sildenafil: Yellow vision - Digoxin Brown vision - Sle 8 :- Kepatetexicity Neurotoxic Ototoxicity et - clot Qrubutee > 97 aR Interstitial wplaig fhould be Counsiled Gets ght Rx “THiorkdazine — Nexolephic - a SOKSHSK9SHSHOHOHSSCHOHHRHOHOHHSHOSHSSOSHRHA2SHHOOE Cn a a a DONNA OO om mMRT tt eee ©0CO82272A2090000'0 Rugs £2 Ber galas Renal Calle qo ES ge tn Fulldoses. . . s QR cuit doses Z avoided. E > avotded : s (20H aoe z HS posed Zz 2 Rigompicie : seared on all mycobacterium foeluding Uses only drug which ack mycobactesum: pros. 2+ Brucellosis < Doc— Port Rifampicin * 3. Legioneltia infect? re Ls pneumonia. %. Staph: Tofectons. + Gemtamycln < Tofectve Erdoca € Osteomyelitis IMeningococtal se 5+ Meningococcal meningitis Cause by 9 Kr menin gitdes > We rngluenza CEPTRIAKONY | Dee - Fit prophylaxis 19 Meningococcal Meningitis is Ceftriaxone - R in neningococca! meningitis 1S ceftriaxone . 2% Doc - In Gonorhea - 3 DOC. - in alt Nefesexial Kofections Za)ae ) 2 duivates qf Rifompen A: Riga pentio - Clorithromy ch 3 clos me 2 macwude G Aaithromycdio 3 + Amikacin AGS 6+ Capreomyao sie #- Kanamycio 8- ciprofioxaco 9: oxoftoxain 4 66's lo - Levofioxada Me Moxifloxadin - 0st effective '2- Cycloserine - 1+ Catt watt sntnesis © 2+ Sje- Newropsychiatite Reaction 1S: Linezolid: . mo-n- Protdosytbess © SIE - myelosuppression . © PLT count -check wae, aac Ih. Ethionamfde- - Drag ‘hich Shows Cross vesistan @ H (wn) 15> Pawo amino Salicyelic Acid . (Pas) = Sle - Hypothyroidism 1G. Thiacetazone - Sie - Hypersensitivity Reactions 5 otdes drugs a a a RRA A RACe ee oe me oe oe | 2790 O0CH8O008 E Ht vfomycto - Aa’ CTota_ 5 4G ack on 8 At 7 stryte 18 Proeonamide- . 3 New dvuge. [9- Tevtaidone Comjugation 9 2 rapleculis 2 cyclosertned Cherneprophylanis Bt 78 | TNH monotherapy = Dose: 10- dom [kg Jaay — Gmons . Ceuen in chit toodose - Y In monotherapy % dase - FR By — 5 mglkg. 24 i6 oot monotherapy inky, combined 2 duge Madaxia ets Doc -> chloroquine. < uncomplicats (cay Doc fA complicated | seueve —> Avtesunale - (cerebral malariacte ) OD St meptoqutoe cte- DOC tn Chiowquine Resistance > Artesunate - Artemesins. gin lo Comiinat Gay Thea Todfo:- ee Plasmodium vivax :- Sensitive to Chloroquine CCQ) P- Faiciparam — Resistant to Chloroquine So Rt Avtesunati (Aer Primaquine:- Role 1n majaria ts Fr Radical & € TO prevent arwlaps: | & given f0, P-vivar. (© hepake, Shines CaEneT Fa sor in P-Faldpatam because it ort has exoenythmodic cycle (9 hepatic Shir Rad Primaquine given fo Single dose in M doy in P Faleipate because Y KH gametoufha) action. (Kin Gamerooytear » . cidal 6g Dose: Cail ey in Pugar- 1S mg [doy Chiden — 0+ 25mg!day,In childuen- O-FS™YING- P.yivax P-Fattiporam Wows “ged Pamaquine- ism |day US mg Children 0-215 mg)doy- 0-75mg. ~ Ceropeeyions yf Dass BrCa Uf CQ Ruistant + Duration of Stay in endumic area - ts SB wks + Doxycycline - > buskers megloquine « =Sazut drug 9% matata. to Pregnancy?! CQ (aun) 2+ Quinine - 3 Proguasil Gy co wef ores I mutes: Act + @ufoine - v 1 oh. wave al Aer ar act Chemo prophylaxis > C& Ca” Residant > Mefloguine - = Chiowquine:- Structure! Ca enter, — D oae prasmadium require Mb fH. wo ne ae) TS ca es ay oe & atigat 19 aad peace A Conjugate (60 FHeme) ogo) fon HOY resto vil “a eens fo deed se. L@eroniyy wm geenondin (Grey cater) Slate ry Coley mavia+ Hb) eget wate FO AR AR RRR Rm mm - ¢CeOeeeeeaooeoooeds COCOOD2E0HC CS Acid Efflux: IL ob ppovk “CCQ Pegstance Transporter ) #2. DEmdy! Ceuit drug resistance 1) Ng. #8 looe! CA” 35 always given to loading dase Fe high No Use: Rieumatotd arthétis CDmARDS) < he HaydvoryCa E xtraintesiinal amoebiasis Camockiguttepatic) DLE ~ LR-2 Lpre React? TwPe-2 CErythema Nodotwn Leprosum) L~ og. moronuctas ss P - hotodermattis. S - ee : a . Sle Acute :- GE fymptom - highly Mitant: 4 Hf oo - Nausea , gasttis along & C@ + Ondanseinn, PPI has Pols ate Long Texm:- CQ Retinopathy. Risk Factors Fo CO" Retinopathy:- SSK Sere Fa CO 1 Age > boyrc- 2. Duration a use > Syrt- 3. Daily doe > amglhkg a > 280mg |day. 4 Of Cumulative CQ exceeds '00 gm. 5. Liver Fallure b’cor mttamobilism Reduced G. Renal Fazjure exevetion b > 4 Concowithent Retinal diseases & Oberity (Co iS 4ipophitic)> te is NitoImidazole- Tinddarole guivatve - : Seenidazale ‘ 5 Doc FA amoebfacis (all forms) - ¢ <> Doc Fe extraintestinal amoebiasis (E14) € > Doe Fh Trichomonas vagiotis. Cxt fe STD Sofat Aastnes aise ued) ¢ é 7% Doe Fo Ongeroble Ingectons é Any Onaxenbic fogection above duaphtagm - Cindamycio € bdow = - Mehontdarole 4 No site locat® - metronidazale . é « Dose:- Yoomy TOS fo. 5-F days. — Armocbiasis é - Goomg ms fe Frlodays- ETA é = Upomg? TOS FA 10 doys - THchomonas < € o Losdigis ng lkg IV Over Thy fotoed - Anaesobfe Infectu ¢ by asmglkg wer 6 brs ¢ = sow o-days Metronidarole ts nok umd 19 Giarctioss. © A é Tinidarle>Doc - 19 Gloxdiosis- € 2 Causing Diarrhea 19 enmurodompromised pts: Cohimoxarole 6 4 ¢ cate spray Cotimoxorote ¢ Isospora ¢ =D CrypreSporidiaais no reponse © Corfmorarle So te & nitazoxanide © pyruvate Fenedoxin oxide reductase, ( Eorg ymC9OHCCHCHOHHCLCOF OOS S890 00 0 AGE Atihnisier B L - Filasta:. ) - Nematodes \ 3) M - Cutodee and Trematodes Filasio. aN Doc- BEC C Diethy! carbaaine citrate) - eupt> Rivex blindness - Onchocereus voluus = Coe- Tvermectin Nematodes Se Doc- Albendarole except in + Entrobius vermicularis Cpiniteotumn) - Mebendarole 2 Strongyloidfasts — - Ivermnectin-Cooe) t * Doc nLawvamigrang - Abendazole . g Viscerat Cutaneous. 2. Doe tm Dracunculosts (Guioeaworn) — metronidazole. eradfeated in Todia Cest % Trematodes Gxteda 3 eee Doe :- Praziquantel rapt 1. Newwocystiaveosis — Doc — Albendazole +s 2. Hydatid disease (€-granutosis) -~o0c- Albenda role 3: Liver fluke. lofeetion (F: hepattea) ~ dee- Triclabendazole.3 Lamivudine 4 Ofdanosine S + zaleFtabine, 6. Emtwertabine 4: Abocautr —_e—_ 4 @ 4, pntisetroviral Drags ie ~ e é e fe fe cD yas ae expe Senabne els a) > Human colt « e 4 e a ceostde RNNRTIS 2 Nude =O { tesegzanscioien © 9 teats cr oH om Raltegrede cou Ber enone €e@ ore ser . ¢ @ oa * . PO Recnterietis Ridovudine +St0vu etiseasl Ha ressdesas on dine vattach same € Site. So not used. oA 2. Cross Resistance. tPF) gle: Pextpheral nusropatry (Mmox T Stavudioe » VY ee ; @ Pancreatitis, (max € Odarosine) 6 e; © 1 Ad A. NNRTES = Samana Se + + Rashes e © €g- Nevfrapine en e 6 E gavivena o|z in pregnaney - dus to Tevatogenesty: ce E tavivine 2 e e Detavirdine- e 6 @ @ & Protease Tahititor . ef . . post : Lt Potent — Ritonavir (mos e¢é ee d. d potent - Saquinavte Cleat potent) 2 e e e Sfex & Lipodystrophy: - e a Tq Hy Choluterol: e . . as atherosclerosis: e é a fh vise ee ® Sidinauis - cause Renal Stones. ee ee Acyclovt °c > Prodrug: ; ; ° @ > usu: b HSV Fafections — HSVT & ASU E — Doc. Aeycloutr. e ef ; Dose - $00 200mg SHmes o doy. of ‘ ; iv Ch: Pox eg 2: VZV Infection + HSv-in Cause vs ee os Dose Boome 3 Himes a day Dy e e ePA Acylouir | Ganetdovis sistant © Doc - Foscarnet- Antifungals I. pntfungal Antibiotics « Crug cetoined from Living organism & acting (On anethu beng organitm . & subelasses :- B. Polyene safbiorics ¢ 4- mnuttibte double bonds) (systemicaity used onl) a 1. Araphatetantic? Qmobetstefo ~ 8 - wystatio eee) eh Hamydo Topical use ~ ratamycta by binding 40 exgosterot in Fungal aut Pees Iyenes ergosteroi( Fagad Polyeredrug —| 9 isortented ChMsteroy (Hamad € Pharmacokinetics. f Give tv sisson ‘ Qrientat® is Cet Premntion of a. tex i¢ water Tosotuble F for this, Prepared é 1: Amp- & deonycholate . 2 Amp 8 Collofdo! dispersion Lépid- complex) : BAmp-& Upid Comper - Bb Toxiaty by « @ Gara 5) ‘ 0 : 1b praant organs from coming ia Centact aug 4. Better tolerated. tolerability ¢ 3. Metabolind 19 Uver ¥ metobolitu Our removed by Bile a SCOOHSHSSSHSHSSHSHHOHHSHOHHSHSHHH9SOHOROHSKRHGOOECe eeeeeerccccoccces e@ee0e ©0200 Fut doses 19 Renal Failute. ott 15 fe, nadhusrorn cos : % ain pF Uses:- 1 AN eurgot ingections local infections - Paola Prete Fuegal neato. usually, Doc. - Disseminated | infections > Can be given to Doc 1. Kala azar - te ht i itselg- @ Risk: Bene SJE Amp-8 tS highty nephrotoxic drug selg. Gepend upon “es Sp Benepe A = Amp 8 avoided 19 RF unless there isa Lge threatening Fungal infections. a hypokalemia. u hypomg: 3-% Pte on Amp B , give kt supplements ( Hypomg- Pat thal Seucte) q@ Anemia & Hypessensitivity Réiactons- Uc Benzofuran CB) Heterocyclic Renzafuran. ): Griseopuitn 1. Act by bioding 4o p- tubulin. 2 Accumulater 70 kerertinocytes: to. Dermatophytos?s 3+ ayective Y Not used row bjos Y ' PSE 2. T ong interackon. RNC oeae 1 Caspofungin - 1 They are Fungal Cel welt Synthesis © De atwaye given ax iv Infuston S03 a Shott T te 3 Used ia Disseminated infects 2 mica-fungin 3° Anidulofungin DwrCandidiatis Diss. Aspergittosis.