Bee caer ae ten haa fen OHO - ghmulated oy B-b.2 8,» Be oo C92. Soe, ViTaMing x ENivamin= is “Teoria” @ Function, oO Co- enzyme 4 dehydrogenases ~ Help deb yerenase. + == | © Mainteunence 4 rreman| pathusait ‘ { Causes OF Derictentcys: d- Chronic Aleahol intalcers obxiption 4 | a. Eating poliche. aa 13 Eating Polisned Rice, | @ Fentares Of DEFICENCY # lactic Acidosis s- “Adult m Lactic acidosis due’ to B, deficien echildal lactic acidosis dus to dekujsrogencge achelencts B eek Ben Tere \otume overload. due ta Sco K Dy, Ben - Beri g- “Nevo pathics”dusty Wy Kovsa- Kort : Confaquiation® Fogetting obsut a parhculay Wing, y ia) ae a deledla 4 Yen fo 4 ddhia lie WD Fl oa memnony } - Psychosis: loss 4) contact 2 weakly No- Insight | No Compliance. % Weanne’s Encepuacopatiy 1 Aloxia. . Nystoqmuts + Opthalmopleqia * Ponnesia | [Chenic Alcoholic PL ¥ Rood Glucose: evel | Dextose canter ing liion 4 Rynvets production | Sudden pyruvate Symatien Xesulbs in By deficienay ever io | | =D So thin pt, shovldet be te dexinse water immediately lack Ws 6, oth wmjection & Bi, to \ $k Prevent NEMO loss. | .Wisi HWiemin-B,} ~~ Rieoruavins ah, dehydrogenase » Fenrures Of Tericiencys- \y Chilloses / Stomatitis 4 crack of aay soon & oe \ooasdeens- a, onde 2 pen ere colored = Fonque 3) Dewmnalryis Mitanin- B,| ~ Nise y= » Niado pet ee 2 Essentiab o | Amino Add le Keatunes OF Dericiencte i \- ¥inoke 4 niacin —> Palleqta a- ¥ Reabsorprian 4 srypnophan—> ocnup Sanavern -Diowhea + Dementia Dermatitis * Deatn | @ funterion + Co- enzyme % dehydrogenase.Role i9 methulonin amino-acid @ Couses De Dericienct, INH sIntake 4 isoniadd (anti TB dng) e TH OF DeéFicien A. Microic Anemia Acquiced Siderobiost Pinemia A. Homoaystenennia f. micmoytic anemia can be causedby lead paiscning a Be deficiency.‘ > 0 SOURCE a2 “Geen leafy vegetables leCouse OF Dericiency 3- O intake of qreen- leafy vegetatcles @Prnti- Epiteptics~ especialy Casboeapine » Nelpuvic acid © Immunosupressant et anti- cancen (metherexa®) \ @ Function | > at Nhgristac sywtce (ir pining a 2 Closure anevior + postemint nea 3) Helps in methionine =~ metabdlismn (one caren metabolism) joFentures Oe Dericieneys” { \- Megpidolaske Anemia | 2- Nestal 4uloe defecio © 3- Homocysteim emia. =p>mcq |9. Which Vitamin | Fellic Rad 4 ut Bins eke: is Nematopaeitic. vilamin? Ba thot agentes neDUE ern - sg Mipamtin- ee Metny\Cobata rain: @ Functions —3- a + Responsible for biosynthesis of, purines +a pyrimidines by Converting mactve fellic acid oD active fm fotlic- acia +lk is aso cated as “hematopoeitic-vilamiry | + Methionine metaloolism leading 4 Homocysteinernia for odd catloon Fotry aid metabolism jeCauses OF Deric JENCY Ay} meak Make, so Hh can be seen in | a Pernicisus Premio | d) Inflammatory Bowel Disease nw Crohels arserce A ileum dut to vight hemice hy Right nemicollectomy |S Diphylobotinivm —\atuen Crape-usorm) @Fentures OF Dericiencys + Meggloblastic Pinemia 2. wha degeneration of g inal cord + | vilamin- By deficieney ‘ OC 3- Pimnesia ee deficiency con couse Suet S- Homodjsieinemia (-4y as (ean cause Yeuew_) NC a | ~&® enayme ot met! melon) co. A mulase, Co- enzymef. qgconac. 0c ' Alesorphon of YM Ank- oxidant Rest - Transtationel Modifica tign- Hyaoxyianon { of \yina polin § collagen Fier—> 4 strong of, collagen” oFenrunes Of Dericientcys OSCR % Bood vessels - EASY Brsitinihy Bleeding Time & Veet Guen Preeding Dentol DMonowmnalit} Beelelala «Bone Por Bone wealuress @ \an- deficiency Anemia OFPisk oh AYnerome~ RETINOL Reti~eL = ReqNOIC Acid 3. Maintainence of epithelivn 4. Reproduction ey s. Brig Ant-Aene for modulo ayche gone Song C™ 6 Ane. Oxidant . Bae F Deficiency: 0 ey Mani fectatio of — Vitanin- A dchichenay.— Nignt blindness _ ' | Xeroprtnalmia (Dry- Eyes) 4 Coneal U\cevation i Bilot Spots hon: @ Gouin Retard | ® Vois- loss @ Squamous melaplasi Epithelium — Recurrent © Anker Hib Q. © P Risk OF Atheroma Lrmation ie Cause oF Deficiency + | d- + \ntoke | a. Fat Malabsorption | © Feohiec OF HYPERVITAMINOSS.A sit 4. Hepatocesular damage 6 Onjness 4 oral mucosa. a. Popasia 3 Bone Pour 4 84s oh BICPr Nausea, vorifing, Heache, papiiedma on Wundescopy, 5. weight ~ loss| MITAMIN-D eAcTWATION of WED, ye Dehydvo onoleshole Uv- Radiakon sun ALCEFE ROL CHOLE Liver J 2S- Hyaroxylase holecodce fevol 9: (PTH) Renod (Pct) | 4.- % Hydro xajlage v > olecalceferle. (Aetive— Foren) FICIENCY s, une. 4. Leen a. Liver Filo: 3- Renal Failure 4. \ntoke, 5. Fak malobosoption i : e So \ dud @ SOURCE s- mill. produdio On GT Tatsorption eh Cot a PO,” Som Git on @ Efeek M Aepesition Cott Old bones:- Bene vesotphon POy io news bone @ Efe dn ladnen XeokHYpovitaminosis HYPERVITAMINOS\S or RO,” ® Cot 2 PO? Childiens- Bickel SIS sh Aypee etna Adult s- Osteomal acia oe se e[Mitwmi-E | oc. Anh- Oxidant OF Deficienays- increase Ase sh A¥heroma formation [vk |. © Causes OF Deficie sy Breast Keeding 2, Broad. specnuin Abx & Fat molabsosp Pint-Epleptic as Phenulhydentoin wt ip is Function , i 7 | © Post - Wanslation rnodification wl T= Catboxylarion af). vit-V dependant clotting Factor Factor: WM, vin, Protein © | Pokuns] mes ~ Requited + the achvatien Faurors wie > o Feetures, 1, Beeding fon oie side ~ Ralonged CloHr§ “Time * 2 Pronomal Exminsic Patinwscy aw PT prolonged, @ Prnti-Dot ef, Warfarin+s] Polysaccnvide ———_} Monosacchiide (\ntestined Lumen) Protein —— Pino Acid | . Upids — FA CHO — Glucose LL ome] Menosacchride. ——> Acety) co =Amino Aci d —————> , Fathy Acid - Glucose Guucoge G\yoolitic Pathrusash in Jute Cycle md Connmnon Melabotic Patfayscuy | NADH Wnet_membrane of pritochondhis ATP Cleckhrorn Wangs pore chau® Giese | Fructose @ HMP shont @ Kreb’s aycle © Electron “Transpast chain © Glycogenesis / Glycogenolysis @ Giucogen Storage DisotderWYCOL LUCO. $ 8 Ys Hexolinase G6 Rsphrale se- Phosphoenol Pyruvate Let J Payovare Winase. Emuyme POR aE Soe Stale Ge [Pyrovote | Malate <= ¢ Pyruvate dehydrogenase | [ic a] 4 _GLULONEO GENESIS e | * Foxnation St Glucose fron none Cats Wydrdled: eomponen's” ” | | Alanin Glycerol Lactate © Silent Mepatocyles Beer aransk“eS he slF some one is SF as in Addison disease, fh Wypogiycemia on St¥ess. =p Anaerobic Glycolysiss- : sPyrovale wil be converted intD lactic acid > Pynwale winace Deficienoye- san cause chr Hemolptic Enayme. => G-6-PDH - me Deficienape- . Sale Neve a Aner, + + Heing Rody => Pyrouate Dehygrogenase Enzyme DeRciernert g- o Lackicacidosis (inskad ¢, cametting into “actey\-Con, jo #* CIF. child will present & Pen Hila Y locke - acidosis “J nae ae let og => ATP production in Glycolysis e- % 6- ATP mY Glycerl~posphate shute % 8-ATP Malaie shute(mink) (acise ) Gat-macora) Gplackose. Q\ucose Golaclanase q Gplactose ~\ - Po, GL PO, uridy) Thansleqse. | Glucose - 1. PO, Glucose- 6- PO, Glucose Glycolitix ® AACTAS EPICIENCY e— * Con be Congenita$ © acapived + Podominal discomfort + Flatulence,@qPe- mature cataract jahisry 8. No involvement % liver a Brain wdessanged LFTs, 4 ved darnage, =eneniod ye fardation. : @- Hyperurecemia + Gook due 40 accumulation OfGanic posphate (sta G- uridyl Hransferase) 4 Rix ATP will Mor occur,ee Fiore vinase (- Fuctose - T- PO, Pidolase— B DHRP Qugoraldehyse e Aroorase- B_Derreienc¥e % Features s- -de-wanged LE T's » Renol Feature -Hyperorecemia 4+ Gout@ Ribose - S- PO, —> Fornation 5 -nudeohde ® NADPHN % Function of NADPH, in Heparooyies? R sible for he. biosy>*hesis obs NeDPH, in WRC'St : free, wodicols, for 0,- dependant nish @ Ane help eh % funchon oF = Fote q NApPH, Raed + “Elimination of O:- fee Radicals, ‘ Guwcose. G-6-Pdy Napp af iY G-6-PD Hydrogenase ¥ Ribosea Algo Known oS % cite Acid Oye FFicavboxWc AA © Common Metatolic Vatrosaus le LOCATION. Takes place in covtecnondiiol ena hx e END- Resuct, Rcehy\- Co ——> CO, + H,0 + NADL a lo STEPS. Puswate ae Oxatale - / Malate Fumarate Ketogiuy Qlotexate,© Succinate Pe erone a | - Also Known as ‘Complex =I" a Present in inner- mnem\biane of enitechondvia. > Hon - containing. anolecale i a cell: - Hemoglobin - MUoglobIN + AytDelnyore.Takes place in ianet- memiosane ° End PResott nape, ——> FTP | 'e Steps a eaytodnrmme b/c. complex - Til 00, | nee Casfochvome alas (44) complex -\V ATP synmnase & camper hy mikdclhondia,: etechon transport will toe | of NADHT—_> innitnit Mere ayete Pyrvate not converted into rely) - CoA Ryrovate convert mo lactic Acid @ |nerors OF Evectront Transport Cuan, Cyanide Phisoning ® co Peisoinin g @ Suceynl Choline € Halothanea Polymer of Glucose 2 Cam, be stored in: cb Liver a 100 qn Lib Svelelol Muscle - 400 gm Lae Function in Liver g- User glycogen povides qiicose 40 tolood in cose oF Wyperaiycem a | x Function in Skeletal Muscles | Retetol purscle doesnrt Felense glycogen for Wood. Ciycogen is used Io} Sketetol muscle? Yhok | Provides Xnem = energy in cose 4. ooh o Source DE Blend Glucose O Dietary Glucose. © Gluconeagenesic @ Q\ycogenolysisGuycoceness £_C ™ ° [Cevcoces} , a a Glucagan Givi | - PO, INsocin | i PO, fDisease Enovme } Features x Von- Giek Disease. Glucose- 6- posphatase + Severe hypoglycemia lactic acidosis a Hypentecennia, a ' Govt * : + Hepatomegaty . Hyper lipidemia » Shot Shahure. . cardiomeg smusde weoleness -Beath by l= Years emild hypoglycemia + Liver enatgement * Anderson Disease ‘Infantile Hypolonia + lived Ciwnosis » Death by 2- Years * Mec-Ardte | il be He's Disease 5 pronase Muscle (skeletal- Yrubscle) in Glyogen- Posphowlase deficient in “He patnaytes” smusde famips 4 Weakness On exercise -mild Lasting Wypogiycemic + Hepatomne g » Liver - coalDifferent Amino Acics Metabolism Disotders esis + ProphuynasPowMeRization! B focen - “Proven Lon + ata |Conwerten INtO -wiaci a leery Fy Peni sence —o - Tyyosin Fate OF Amino- Acids. ' CarABOLIZATION ~4—— Cattcon-Skeleton — cooit"> -Glucese Ketone Fatty Acid HOO, C0, + Hie /a THCOs tN He actimnldal Ps | Catoony) - POy Syotrase - 1 Ew Corton) POy ———» Opoic-fleid ge i é & 3 ' fans Sse Cott Penajloce £ Onin = a | Cirnsling | Qiruline CyropLasAamM © Location : “Hepaiooyic’ % START ws in mito chondria Mepatooyte. | # Completions ures fownation in. extplatnn of, heparootte 1@ Fonction: Conversion oh Na 4qurea ee e ies pe Sane @ lead Prisining @ Femcnelatase deficieng ~! Congenital Sider lash Acennion on Deficieny Anemia (ap Haemosisena present 10) (7 wrihdnendvia. thats wal (ee sidevoblastic | KC finennia Wuavaiinacre © THAAsemiA ve Acute _lrenmirrent Promivuias «CAUSE, deficienay Patpnotsitinege? x Fear 4) GIT ~ - nausea Somitting auile cledominal pau Parient may have multiple leprotomies € noting fsuind. -dut Fo uibidh sroutiple | SnOX aks ON aAntenior aoagominal uaadh.. | 2) CNS w -Newpathy - Soot dyop ewisk drop Psyainic - mranife slabon:- - inxich) = Para noiar (extreme suspicious) | 3) Port-wne Urine ah ° Yu Glucose Yu HerninGlucose, Gqyeogen by WweLIPOPROTEIN, PARTICE arund lipids. Chylomiewn Cveceiie annem VLDL cory be IDL mo: TAC LoL ee HDL vee “Dietary TAG + Cholesbol Synthesized in intestinal mucosa | | e(/ VLDL ]- - Newly Synthesized TAG + cholestrol | Synthesized in liver | =p[RBad- Cholestl|~ Promote Athermo - formation Chujlomieron; VeD ty IDL, LDL ave. ee 9S bad choleshole (offense) % E00. GHoLEsTaDy|- “Inhibit Athewerna- Formation HDL - (Dérenswe) ° |_ + Olive- oth Bounce OF HDL - low- dose of, Alcohol — LDL formed from ae by addition of cholespe| vis uptaken loy Stervidogenic OFgaNS t— iy Nivey 2) OvariesAPO- PROTEINS Die APO-Byy ~ wade 1h Gan ea + Cholestol | 48 le in — Po. Pe na |. a ee testo 2) APO-Cy, = PPO- C, > stimulation 4 I TAG > Choksho! | | ton wo ee line 4 hore 3) APO-E | espana | PPO-E > Re-uplaken ley liver, TAG > Choeshole 0 PPO- Boo ~ ['npo-8,,.—> mode in livew . ly APD- Cw BRO. C, —> Sein Hebei BDAPO —Bpo m1 |-RPD- Bag Uplaleen my ver TAG = Choleshole TAG < Choieshole sy APO- E | © BPO- By uprauen by liver uplaieen by liver,- Farniiad Agochupornieroneenc® * Causes. Liproproteun Lipase defideney Aro c- iL deGdencs & Feohue gs) Putosoonat ~recessive disorder 2y Vuperrrighycevidernion —> > 4000 *Livre Wa |2- Stoned Hyper clnoles Her mem je Couse Deficiena ot, PPO: Bro Recepiors oa hi % Feahes, . futosomal Dominant disorders - ischemic features 10 eorly age Aue 4o athena fownation. “phe esepsesnmerpee - kan¥nernas of —Adluliase Tendon » Cornea) Prous : + Xamthe lasenas DRvgs 4 cholesho} lee ~ Digs stirrvlating Upoprojein Lipase, . “ Chlofitiate e - Gemfibmri} STATINS’ ; % Rosuvastatin : Cholestyraming * Abmiastatin » @lestipate » Simvasta in$ | ide- Effeck s- fiver damage: neuer use niacin = stako. 2») Flashing + pravitis, by Avelease Prostagandio —> Fe = seid (Sele 3) Hyperurecemia + Huperglyceenio.| | A- Aceby) Co-A : | t | | Aceto acetyl Co-A L HMG. cof] synrnose LiveR HM - CoA | 4 L HMG- CoA Reductase «— Binal | Mele Mevalgnate | $ | | Squalene | 1 Lanosterle _4 en 0 te 4 Fundions + | Ay levteqrod Rat 4 iosno nuetene \ay AN Sewid-Howmones ave denivotive 44, omen |3) Vilamin- D is a derivative choeshole 4 AY bile add 4 bolle sob ove solvates ae Onoleshole i Iplood, cnt | os tee is $ dielany cH,0.Pip - Srorace Misorvers 5 eee Dense T Guzyme | t on |’ FenTures a Nimen- Pick Springomeinase i f ina — Bright F Feorys Fics si A Pets Go. rae ¢ Gaushet Disease % Kenge’: Disease # Melochromatic Lesko! #e Taysoch- Risease | Hexoscrninw» Rosphohdic Aeia 1 a ily Risphotidy| Ernanclamine 2 c O-FA i. oridy SphingoGluco lipids: ws €-0-FA Posphetidy! nosito! * Cesamid + oligpseccnide = Glob sie) = TAG inp Pespotidy) Serine vp Poigroty) “choline. Dipaten Tapt ay w) Beprone Aa Giycerst Paphbtic Aid ) { [Ceapouris]Syathesize anhipodies pe ~ Anti phospholipid anno: Prnticardiolipin ' Ann CARDIOLIEN Arti YNDROME 4. | - Pintipospholipid a \ - Feahwes . | U) Recuwent GA in young fernole yj a, Reanrent adeortions | S Ihingo- hipids - present in plasma- ymemnlotane cou Wot ne a agama 4 | syseen # Ceul- cligestive 4 1s lysosome — + AN G& sphingolipids ate digested the lycrsamal en : i in Sood Neciiles: "3 " . | a IE lygesomat deficiency, ik vill xesolk 9) Aye | stoage 4}, sphingolipie d — aac Ao looxst 4 j Nocules : + Macrophages wee eae! do" eagutt anesei paride, 4 mMaorphages with, englfed Ssphingaipids wil Ire Venouinn as Foary cols Tese foam cals ai deposit in different a 4+ will Gre S4mptoens occ oxdingly—— LipiaeT Gee -OxiDATIOR | @LOCATION g inner memlaane of mitochordria | @ FUNCTION, -Rrformed fo convert Fatry Acid ——> [A hy con] G | Alucagon 1 * | Skeletal -rovrsche FA- Canotin | | > (elzll Cogan) FA. A Cardgiioe FA- earnatine Catnaing Shoe47 ¥ Features | Exeicice + ow fok DISORDER | Exeyne Dericienc] « MYOPATHIC CAT unt be © Prolong, high- Covenrusprane oil CAT deficient iN We yitochendtia 4} Revie —> -Oeee S DEFICIENCY Qeletad masele wpenigehe GeCeSaaay _ Myoglobin uted aMusde foiopsy itl sine ees J MCAD | een. oe oNo Ketone odes, ®eriaency [Fa-CoA DEHYDROGENASE Nii WES ae eee TR a ee (M-caD | . | deWiydvo genase edison - chains acehy-G e Fame Pe foceTL-CoA A, CO, + HO + NADH \ v 2, Cholestrole 3, FA hy Ketone EAUcorAM levecuraR, Geneneg ” OStavcrure Or DNA @ Ko€PLICATION @ _IRANSCRIPTION } Gene - Expression @ _IRANSLATIONNTROGENOus- BAS! ace are A- main Aypes of +Riconuciestide- RuA detelop + Deoxahnonucientide.. DNA desetop Hodeotlide Larger Nitrogen Base WO © Adiaine + Quanine aig Nitngen 0 ee in + Uradi\ - Piéent id RNA inslead oF “Thyamine . TWiyarnine@ NUCLEOSIDE. ¢- NUCLEOSIDE a ADININE = fdenosine deo ss Ribo be _Aeotia poe = Quanale Co “pe onyseo = CNTIDINE < Cae CYTOSINE = CYTIDINE < 2,, penne oe = URDINE < \ Ris pyeioe ye TRNAMINE = THIMIDINE < z pleat oe NucLeoTiDE -- + a ene = ete Ade Bs + FAdenome. =e | Poa _ Guanine + Curanosine = feet CYTOSINE + CITIDINE = CITIOINE mono} oposphale ~ pono pospnate. hy ae Timing + TYMIpNe = Tyrie | op ’ A * ee + URIDINE = UndineadmA 16 @ dovble Shanded rncleaule Complimentary, | Dr vacteatles 3 anhi- pavalte) ore packed oH Boh sands ave tp cach other. 5 of Histones- sively charged protein.DNA 7 LINEA ae Can he seen ia —can be seen Eutanyofic - cell Procanyohic - cal -Vnoum os + -koousn 0 [PLASMID] during Hone Cell - whey west Foun ¢ 4S | x]PLASMID|- ray be 1 resent in tne Mitochondvig, Se of cal | +25 genes ave present im plasmid * Strocture OF Curomosome | P Seaivls ~ Prolein: Dw wits on thin Ratein 4 foren 0. Onverneusrne a“eDeenimion’,- % Famation ef DNA fr DNA” jeLocation ge Nucleus o eukaryotic - cau) sepiéatian -CYtoplasm s prokanpphic- es + dna-P. prokin Vv ORIGIN oF Repucaion | y / Replication Rubble. Sypthesired by Rrva- Rime Reticase W_iii) Helicase Ratner Vieakedouy of huydragen -toor vw 2 Shands. 2) Formemion of RNA - Ramer s- «© Prmose will form RNA primey e RNA -prirer is a Smal stand molecule composed ef 4L0-rwcteotides- y Formation oF LEADING + LAGGING STRAND , +Tere's a wie of sMe uatt tad From 3 40S 4 Le wit wate from S40 3, VE ail - xed vad proof VE wai Show endonuclease a avring foo\t found. a Remeval_of Rvp Pewter + DNA polymeras Lis tesponsille for ~semoved. g. RNA primer = DNA molecule.Gene So \es\ ° winidn 15. | ¢ Senotiest Gant ¢ DNA < SespHnsitore for We — fexenation of . esse Qt RNA” \cp0 — \SD00. nucheohades. [Notes te is composed af L000 : Dow |) Lpstaiges om {ena eS Ants Sense - stand er” rere yen factor ~ Nansoiptional Sackue (protcaryotic) Céoreoyohic cel) [ paig : Somme 4 RNIA- Palymonac at |, 0 Promotor Prox will alwsanys be on vp-steam end o enypmne . je Wanseription wilh stat fm vp -sWeanm end 4 Jecrimake oF | dovx- Stearn end. 0 Sence- Shand ai + Template stand + tive Shand | + Coding Strand | |e Prnti-Sense Stand « Ponti — Temptate » ° ive Stand + Nan- coding Stand0 Locnmon! ,_ \) Nocleus, no : : ity Cytoplasam ead » Steps o _) Holo~ Emume Formation : Bi 3 i fey MRNA polymesace will enter toto tne Gene 34 Promnebor 7 iNew Yhrough TT Gaca o TATA. 3) RNA PAYMerase “afjer erty ual cress! wel i) \ 4) Then RNA polymerase with xead From 3'-S' end. Sy RNA@ Polymerace. start » [ennai a : ~can be > 3 Nes: » Yap loop Foccnation, 9 “ONG: Metbai aS. RO act el a De Fodor, DependantSPuansia inwons will be Aemoved fron mRNA + Exons will eunile = CRemoval <4, unuseful portion)