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Global institute of medical sciences

Global institute of medical sciences

1. www.gims-org.com
2. www.usmletutor.org

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    Biochemistry high yield part 1 Biochemistry high yield part 1 Document Transcript

    • The medical biochemistry - FMGECARBOHYDRATE CHEMISTRY:-  Formula:- Cn H2n On  Glucose and mannose are epimers at C2 carbon  Glucose galactose epimers at C4  Enantimomers are mirror images to each other.  α and β cyclic forms of D-glucose known as anomers  C1 is anomeric carbon  Benedict test reducing properties of sugars  Sodium amalgam is used as reducing agent.  Reduction of mono saccharides gives alcohols.  Aldose reductase converts aldehydes to alcohols.  Fructose is converted to sorbitol dehydrogenase (liver)  Monosaccharides gives needle shaped osazones.  Maltose gives sunflower shaped osazones  Lactose gives powderpuff shaped osazones  Maltose (α1-4) (glucose + glucose) – maltose (hydrolysed)  Lactose (βgalactose – βglucose) (β1-4) – lactase (hydrolysed)  Sucrose (glucose-fructose) (α1- β2)  Glucosidic bond- bond between monosaccharides.  Sucrose is hydrolysed by sucrase/invertase  Dextrins are breakdown product of starch  Inulin is a polymer of fructose  Glycogen and starch are polymer of glucose  Inulin is need to assess GFR  Dietary fiber is cellulose (β-glycoside bond)  D-glucoronic acid + N-acetyl glucosamine – Hyaluronic acid  Keratin sulphate keeps cornea transparentLIPID CHEMISTRY:-  Saturated fatty acids does not contain double bond  Unsaturated fatty acids has double bonds  Linolecic, linolenic and arachidonic acid (PUFA)  Deficiency of EFA – phyrnoderma (toad skin)  Arachidonic acid gives Eicasonoids  Unsaturated fatty acids exists in Cis form  Hydrolysis of triacyl glycerin with alkali produces soaps (saponification)  Vit.E is naturally occuring antioxidant, superoxide dismutase, uraseGlobal institute of medical sciences www.gims-org.com
    • The medical biochemistry - FMGE  Purity of fatty acid is checked by iodine number  RM number (Reichert-Meissl) – to check purity of butter  Phospholipids – free fatty acids + alcohol + phosphate + nitrogen Base  Lecithin – choline ( nitrogen base) - ( lung surfactant)  Hormones like oxytocin and vasopressin action is mediated by phosphatidyl inositol  Sphinogophospholipid :- cerebonic acid + sphingosine + phosphate + choline = sphingomyelin.  Phospholipases – A1, A2, C, D  PLA2 (phospholipase A2)– give arachidonic acid  Ganglioside GM2 accmulates in taysachs disease  Cholesterol –C27 H46 O  Cholesterol has ohg group at C3. Double bond between C5-C6  Ergosterol is precussor for vit.D  Zaks test is used to identify the qualitative analysis of cholesterol  Emulsified fats in the intestine forms MicellesPROTEINS AND AMINO ACID CHEMISTRY:-  kjeldahi’s method is used to find out protein in biological fluids.  the amino acid glycine has H as side chain  alanine has –CH3 (methyl) as side chain.  Cysteine and methionine are sulphur containing aminoacid.  Aspartic acid and glutamic acid are acidic aminoacid  Phenyl alanine, tyrosine, tryptophan –aromatic aminoacid  Alanine is glucogenic aminoacid.  Leucine and lysine – ketogenic aminoacid.  Monosodium glutamate intolerance causes chinese restaurant syndrome  D-penicilamine- used as chelating agent in Wilson’s disease (Accmulation of copper in brain)  N-acetyl cysteine used in cystic fibrosis and chronic renal failure.  GABA-pentane is used as anticonvulsant  Linear sequence of aminoacid seen in primary structure  α helix and β sheath – secondary structure.3 diminsional arrangement of protein –teritary  2 or more poly peptide chains- quartenary structure  Peptide bond – bond between 2 aminoacid.  Sangers reagent – used to determine aminoacid sequence  Sangers reagent used to determin insulin structure  Biurate is a compound formed by heating urea to 180 degrees . process is biurate reaction  Copper sulphate is used for heatin in biurate reactionGlobal institute of medical sciences www.gims-org.com
    • The medical biochemistry - FMGE  Glutathione is involved in transport of amino acfid in intestine and kidney via glutanyl cycle/meister cycle.  Aspertame – artifical sweetner. NUCLEIC ACIDS AND NUCLEOTIDES:-  Nucleotides – nitrogen base + pentose sugar + phosphate  Nucleoside – nitrogen base + sugar  Ribose and deoxyribose differs in C2  Purine nucleotide is Adenosin mono phosphate  Pyramide nucleotide is Cyitidine MonoPhosphate, UradineMonoPhosphate  Alopurinol used in the treatment of gout  5- fluorouracil used in the treatment of cancers  Azathioprine is used to suppress immunological rejection during transplantation  The width of double helix of DNA – 20 Å / 2 nm  Each turn of helix contains 10 base pairs  Each turn of helix is 34 Å  2 strands of double helixd are hold by H-bonds  DNA protiens are known as histones  B-DNA proposed by watson and crick in 1953  A-DNA has 11 base pairs per turn.  A and B- DNA are right handed helix  Z-DNA is left handed helix  Z-DNA has 12 base pairs per turn (zigzag)  Formamide destahilses H-bonds, therefore it lowers Tm  Formamide used in recombinant DNA technology  The sugar in RNA kis ribose  RNA is subjected to alkali hydrolysis and DNA cannot  RNA can be identified lby orcinol colour reaction because of ribose  Nucleolus synthesis r-RNA  DNA converts M-RNA converts protein  M-RNA has 7 methyl guicnosine at 5 prime end  The 3 prime kend contains poly- A tail (MRNA)  The stucture of t-RNA resembles clover leaf  the acceptor arm of t-RNA has CCA cap (3prime)  D-arm has dihyrouridine (t-RNA)  TψC arm has T, pseudouridine and C (tRNA)Global institute of medical sciences www.gims-org.com
    • The medical biochemistry - FMGEENZYMES :-  There are 6 cclasses of enzymes  The functional unit of enzyme is holoenzyme  Holoenzyme is made up of apoenzyme (protein part) and co-enzyme (non-protein part).  Increase in concentration of substrate increase enzyme velocity  Km = ½ Vmax  Km = S (substrate concentration) Km-(michaelis-menten constant)  Km is defined as the substrate concentration to produce ½ maximum velocity.  Low Km denotes strong affinity between enzyme and substrate  When enzymes are exposed to C and above temperatures denaturation occurs.  All enzymes are active at neutral PH (7)  The most common aminoacid at active site is serine INHIBITORS:-  Xanthine oxidase – allopurinol  MAO (mono amino oxidase) – ephedrine, auphetamine  Dihydrofolate reducatse – aminopterin, amethopterin, methotrexate  Acetylcholine esterase – succinyl choline  Dihydropteroate synthase – sulfanilamide  Vit. Kepoxide reductase – dicumorol  HMG co-A reducatse – lorastatin, compactin.  Disulfiran is the drug used in the treatment of alcoholism  Transketolase requires TPP  Streptokinase is used to remove blood clots  Streptokinase converts plasminogen to plasmin  Asperginase is used in treatment of leukemias  Increase amylase – acute pancreatitis  Increase SGPT (serum glutamate pyruvate transaminase) – liver diseases  Increase alkaline phosphatase – rickets and bone diseases  Increase acid phosphatase – prostate carcinoma  Increase aldolase – muscle dystrophy  Increase troponin I – MI (first marker)  Increase CPK1 – BB (brain)  Increase CPK2 – MB (heart)  Increase CPK3 – MM (skeletal muscle)Global institute of medical sciences www.gims-org.com
    • The medical biochemistry - FMGELIPID METABOLISM:-  TG – plasma concentration is 75-150 mg/dl  Cholesterol – plasma concentration is 150-200 mg/dl  Hypercholesteremia - >250mg/dl  Hormone sensitive TG lipase removes fatty acid from C1 or C3 of TAG  glucagon, epinephrine, thyroxine, ACTH – increase cAMP – increase lipolysis.  Insulin – decrease cAMP – decrease lipolysis  Glycerol is metabolized by liver.  FFA from Adipose Tissue are transported to liver by albumin.  Brain, erythrocytes cannot utilize FA  FA activation – cytosol (ATP, Co-A, mg2+) requires 2 ATP  Long chain FA are metabolized in peroxisomes  Tangair’s disease – plasma HDL particles are almost absent  Biosynthesis of FA in liver starts with glycerol and in adipose tissue with glucose and acetyl Co-A  Glycolipids act as receptors in cell membrane  Absorption of cholesterol from intestine is by diffusion  Cholesterol gives bile salts, vit.D, steroid hormones (sex hormone and corticoids)  Prostaglandin exhibit platelet aggregation, increase cAMP and vasodilation  Obesity gene – leptin  β-oxidation – mitochondria  activation of FA in β-oxidation – cytosol  melanoyl Co-A inhibits – CAT-I, thus inhibits β-oxidation  CAT-I – outer mitochondrial membrane  CAT-II – inner mitochondrial membrane  Medium chain aceyl Co-A dehydrogenase, rate limiting step of β-oxidation.  β-oxidation of palmitate gives 106 ATP  SIDS (sudden infant dead syndrome) – deficiency of medium chain aceyl Co-A dehydrogenase (M-CAD.)  Methyl melanoic academia – vit.B12 deficiency  Methyl melanoic Co-A – requires Vit. B12  Zellweger syndrome – absence of peroxisomes cerebrohepatorenal syndrome.  Zellweger syndrome – defect in long chain fatty breakdown  α-oxidation – Refsums disease – accumulation of phytanic acid.  ω-oxidation requires – cytochrome P450 , NADPH, O2.  Ketone bodies are synthesized in liver  Ketone bodies are utilized by brain in prolonged starvation  HMG – CoA synthase – rate limiting step in ketone bodies synthesis  Ketone bodies cannot be utilized by liver because of deficiency of thiophorase  Acetone exhaled by lungs – sweetish odur.Global institute of medical sciences www.gims-org.com
    • The medical biochemistry - FMGE  Detection of ketone bodies in urine – rothers test  Glucagon stimulates ketone bodies synthesis, insulin inhibits  Treatment of keto acidosis – insulin  Fatty acid bio-synthesis – cytosol.  Acetyl Co-A for fatty acid biosynthesis (FAB) obtains from citrate lyase  NADPH in FAB obtained form HMP- pathway and malic enzyme  Acetyl Co-A carboxylase – rate limiting step in FAB  Insulin stimulates FAB –glucagon inhibits  Un-saturated fatty acids synthesized by fatty aceyl Co-A desaturase. Human lacks this enzyme.  TAG synthesis – adipose tissue  Cerebronic acid + phyngosine = seramide  Seramide + phosphate + choline = sphingomyelin  Phospholipase A1 – cleaves FFA at C1  Phospholipase A2 – cleavesFFA at C2  Phospholipase C - cleaves phosphate and glycerol found in lysozomes of hepatocytes  L-CAT found in lungs  L-CAT activity is associated with apo-A1 of HDL  Sphingomyelinase deficiency niemann’s pick’s desease  Deficiency of seramidase Fauber’s disease  Deficiency of β-galactidase krabbe’s disease  Deficiency of β-glucosidase gauchers disease  Deficiency of α-galactidase fabrys disease  Deficiency of hexosaminidase A – Taysachs disease  Cholesterol biosynthesis, liver- 50%, intestine- 15%  Cholesterol synthesis- cytosol.  HMG- CoA reductase – rate limiting step in cholesterol biosynthesis  Cholesterol formulae :- C27 H46 O  Glucagon – glucocorticoids – decrease cholesterol biosynthesis  Compactin, lorastatin inhibits – HMG Co-A reductase  HMG-CoA reductase also inhibited by bileacids  7-α-hydroxylase – rate limiting step in bileacid biosynthesis  95% of the bile is reabsorbed and return back to liver  Primary bileacids – cholic acid chenodeoxycholic acid.  Conjuation of bile acids done by – glycine , taurine  Deoxycholic acid,lithocholic acid – secondary bile acids  Chenodiol treat for cholilithiasisctiatn of chylomi  Chylomicrons has B48  VLDL has B100  HDL has apoprotein-AGlobal institute of medical sciences www.gims-org.com
    • The medical biochemistry - FMGE  Activation of chylomicrons and VLDL requires Apo-CII and Apo-E from HDL  Lipoprotein lipase deficiency – hyperlipoprotenimia type I  Defect in LDL receptors – type IIA  Excess apoB – type IIB  Abnormality in apo-E – type III  Over production of TG – type IV  Defect in HDL receptors – tangier’s disease OXIDATIVE PHOSPHORYLATION AND ETC:-  Phosphophenol pyruvate is 14.8 cal/mole.  S-adenosyl methionane is 10 cal/mole  cAMP is 12 cal/mole  ATP is 7.3 cal/mole  The inner mitochondrial membrane is impermeable to H+, K+ and Na+  Co-enzyme Q is also known as ubiquione  Complex-I – NADH-co-encyme Q reductase inhibited by – amytal, rotenone, pricydine-A  Complex III – Co-enzyme Q-cytC reductase inhibited by antimycin A, BAL (british anti lewisite)  Comple IV – cytochrome oxidase inhibited by cyanide, CO, Na-azide.  otation of -subunit is 12  ATP synthatase has F0 and F1 subunits.  F0 – channel protein C  F1 – central γ subunit, 3α, 3β  Mutation of mitochondrial DNA – oxiphos disease AKA (lebers hereditary optic neuropathy)  2, A dinitrophenol – uncoupler of oxiphosphorylation  Digomycin inhibits oxidative phosphorylation by binding to ATP synthetase 2 blockes proton channels  Atractyloside inhibits oxidative phosphorylation by blocking the adequate supply of ADP.Global institute of medical sciences www.gims-org.com
    • The medical biochemistry - FMGEVITAMINS:-Vit.A:-  Retinol is present in animals in the form of retinylester  Retinal,retinol and retinoic acid are vitamers of vitamin A  β- carotene gives l2 moles of retinal by 1 ’-1 ’ di-oxygenase  retinyl esters are transported by chylomicrons and stored in liver  retinol is transported in circulation by RBP 9retinal binding protein)  rods – dim light vision  cones – bright light  vit-A required for rods  rhodopsin present in rods  rhodopsin = 11-cis retinal + opsin  during walds visual cycle rhodipsin is bleached to metarhodopsin-II which increases C- GMP an degenerates nerve impulse  Vit-A deficiency night blindness  Serene deficiency of vit-A causes xerophthalmia, characterized of dryness of conjunctiva and cornea, white triangular plaques, bitot’s spots are seen  Xerophthalmia leads to keratomalacia causing total blindnessVit. D  Ergosterol (plants) ergocalciferol – vit. D2  Cholecalciferol (animals)- vit.D3  Vit-D synthesis takes place in skin.  1,25- Di-hydroxycholecalciferal is known as calcitriol i.e., active form of vit-D  25- α -hydroxylase and 1-α-hydroxylase requires cyt-p-450, NADPH and O2  Vit.D is essential for bone formation  Vit-D deficiency:- pickets – bowlegs – children; osteomalacia – Adults.  Alkaline phosphatase activity elevated in rickets  Vit-D is more toxic in over doses  Vit-D is transported in the circulation by α2-globulin  1-α-hydroxylase present in kidney and stimulated by PTH  25- α –hydroxylase present in liverVit-E:-  Anti sterility vitamin  Also known as tocopherols α,β,γ,δ out of these α-tocopherols more active  Vit-E is transported by VLDL and LDL in the circulation  Normal plasma levels of tocopherols <1mg/dlGlobal institute of medical sciences www.gims-org.com
    • The medical biochemistry - FMGE  Vit-E naturally occurring antioxidant and it requires selenium  Vit-E prevents peroxidation reactions of PUFA  ALA-synthase requires vit.EVit-K:-  Vit-K also synthesized by intestinal bacteria  Bile salts are essential for absorption of vit- K  Transported to liver by means of LDL  Vit-K is responsible for post transitional modification of 2,7,9,10 clotting factors by carboxylation of glutamic acid  Carboxylation of glutamic acid is inhibited by dicumarol  Deficiency of vit-K leads to lack of acive prothrobin in circulation  High doses of vit-K causes hemolytic anemiaVit-C :-  Vit-C is required for collagen formation  Vit-C is co-enzyme for hydroxylation of proline and lysine, where protocollagen is converted to collagen  Deficiency of vit-C leads to scurvy, delayed wound healingVit-B1 :-  co-enzyme – TPP  TPP required for PDH transketolase  Deficiency seen in the people who consume polished rice as a staple food  Elevation of pyruvate in plasma and excrets in urine  Wet-beriberi – edema – systolic increase – diastolic decrease – bouncing pulse.  Dry-beriberi – no edema – neurological manifestations are seen  Decrease transketoplase activity – Wernick’s korsakoff syndrome  Thyamine deficiency more commonly seen in alcoholics.Global institute of medical sciences www.gims-org.com