biochem Flashcards

Question

الانزيم الي بحول الacytl coa لل manoyal coa؟ والmanyoal coaلل palmat؟

Answer 1

1- اسمهacyal carboxylas rate limting step= ===يستخدمco2 2- FA synthase يستخدمNADPh

Answer 2

1-2actyl co = aceto acyal / 2-aceto acyl= hmg co / hmg coa synthase =((rate limting step)) 3- hmg coa==acetoacetat كيتووون / hmg layse then acetoacet convert to aceton or b-hydroxybutrat

Answer 3

( starvation) depliation oxaloacetat from tca cycle diaptic keto acidosis = gluconegesis= depliation of oxaloacetat alcholism == increas nadh / nad ratio==1- prevent us from make oxaloacetat from tca 2- useing nad for excretin of ethanol no nad = no tca cycle 3- prevent gluconegensis from preventing malat converting to oxalvoaacetat then to pyrovet يودي الي hypoglycimka والموت لانو ماعنا نايسن (nicin-nad) ماعنا تحليل سكر ماعنا طاقه

Answer 4

menomonic=got some add point have understand coorect path hemeحصل على بعض النقاط من حفظ طريق الهيم glycin+succinal co== aminovilic acide==prophobiliourgin =hydroxymethilbilne=uroporpho=corpoporpho=portoporpho==heme قلايسن=امينوفيلك=بورفو هيدركسيل يوروبورفو=كوربو بورفو =برومو = هيم

Answer 5

7 step with 5 enzym important 1,2,3 step 1-ala synthasis glycin= amin iliv 2-ala dehydro=aminovilic=porpho 3-propho deaminas=porpho=hydroxy step 5= uroporpho =corpo poropho = using ((uroporpho decarboxylase)) step 7== ferrochelateas=بحولporoporpho=للheme

Answer 6

1-ala synthasis deff=sideoplasti animia == izonised useing= b6 deff ++ lead poising + alchohl drinking =blue ring 2-ala dehydrogenase deff= sidroblastic animea= lead poisingوالاسباب الي فوق برضو = show lead line in xray=basophilic stpiling نقاط زوق 3- porpho deaminas defficency =acut intermetent porphoriya== nurotoxin =sever abd pain+polynuropathy+port wine spot+psycolgic issue+muscle weakness 5-porphoria cutnia tarda=uroporphongin decarboxlase diff= كبد وجلد =hyperpigment+ photosenative +ethanol + hib c exerbaton

Answer 7

==homocystine==cystothion== cystine /b6/b6 or homocystin== methonin /b12 1- cystothion synthase 2-methonin synthase

Answer 8

كلهم بيجوا باعراض خراب الCT الانسجه القاسيه ويعير عنهم ب menomnic : homocy H: homocystin uria / o:osteoprosis / : m:marfenoied habits / o:oculr change / c:cardiovasculer/ y: kyphosis 1- methonin synthase defecincy= give b6,b12 and methonin 2-cystothion syntases defency or decreas affenty = give cystin c b6 3- decrase tetrahydropholat reductase give folate in diet

Answer 9

decreas pct absorbtion of cola / cystin//orthnin// lysin//argnin==cystin uria= urin alklization and chelating agents

Answer 10

urea came from amonia (amino acid) catabolism protin=converted to amnia(nh3)= amonia converted to urea in liver=then excreted in urine

Answer 11

مرضين و٣ انزيمات step-1-amonia(nh3)+ co2=carbamoyal phosphat useing carbamoyal ph osphat syntahase == rate limting step مافي مرض step-2- carbamoyal phosphat add to orthinin to form citrulin by orthanin transcarbalays = increasing orthanin +carbamaol + decreasing citrulinمرض ١ ==+ amonia (nh3)=== hyperamonia symptoms= 1-asitraxis //2-cerbral edema =ataxia vomting alter mental status blured vission slaterd speach -last step argenin hydrolysied to ornithin and urea useing argenase if defecent =diplagia +abnormal movement +growth delayمرض 2

Answer 12

urea cycle step-2- carbamoyal phosphat add to orthinin to form citrulin by orthanin transcarbalays = increasing orthanin +carbamaol + decreasing citrulin ==+hyper amonia (nh3)=== hyper amonia symptoms= 1-asitraxis //2-cerbral edema =ataxia vomting alter mental status blured vission slaterd speach

Answer 13

lysis arginin to orthanin and urea causeing hyper argenin بتجمع بالعضلات بعمل شلل ثنائي spastic+ abnormal movement بتجمع بالعظم بعمل growth delay mild hyperamonia protin free diet + argenin free diet

Answer 14

METApod is ARYAL BROken بكومين غبي ومابتحرك enzyme: ARYAL transfer accumulation: cerBROside sulfate==مافي مخ سربرو ع السايد محطوط finding:demylenation+ ataxia +demintia

Answer 15

the GLOB of GOO krabb is out of this GALAXY enzyme= GALActoseprosidase accumulation =GALAtosbroside finding=GLOBID CELL + Oligodendrocyy distraction+Optic distraction

Answer 16

NIMAN is PICK ia a BIG FOMY SPHEINGER enzyme:sphino accumilation=sphin finding= fomay cell//(big)= hepatosplenomegaly chery red macula

Answer 17

my FAVEROIT CERAMIC IS GALAXY HARPRING ON IT enzyme=galactossidase A accumilation =cermide thio finding= harp? *hypohydrosis+angiokertosis +renal f + perphral nuropathy*

Answer 18

7 diseas metapod krap diseas= metapode is aryal broken pickomin الي بشتري aryalملهوش مخ nima diseas= nima is big fomy sphinger نعيمان اصبعه كبير وصل من انفه لعينه =big=hepatospmegaly =krabb diseas=kraap الاقوى بالمجره مابشوف وماعنده اعصاب= gala+side =febry diseas= fabing on cermic galassis بعمل ضعف اعصاب +فشل كلوي وكل شي=gala+ side =guncherdiseas= برو معهbig gun طخ عالfemuer =glucobro+ side= avas uler necrosis+ osteoprosis+hepatosplenomgaly tay sachs = gana (gm2)of six small jewحرقو اعصابنا انعميت= small heptic + hexoenzyme

Answer 19

برو معه gun طخ على الfemuer enzyme=glucobrosidase acumilation= gluco bro side OSTEOPROSIS most commen lsd gross femral head

Answer 20

phenylpherine=tyrosin=dopa=dopamin= nor epi=epi dopa=melanin=tyroniase-albinism بهاق normal count of melanicyt without melanin شعر ابيض

Answer 21

affects nuro mss usually albensim dopa = melanin useing tyrosinase - --- x-xxxxxx- xxxxxx----x- phenlketouria phenlyanlin convert to tyrosin by ((phenyal keto hydroxylase)) + BH4 MOLD musty odor+ epilepsy+ lose of hight+dermatits --- -- --- - -x-x-xxx-xx alkaptonuria= tyrosin convert to homogentic then toayloactet by ((homogentic hydroxylase)) = then fumrat= if homgentic defficncy = alkopoyinuria skin + joint = pigmentation (skin + urin)+arthrlgia

Answer 22

الكحول ماده فيها h انزيماتها dehydrohenas 1-thanol = actyal aldahyd//use alchole dehydrogenase =zero order بشتغل بالوقت مش بالتركيز لو شربت كثير بصير تسمم بستخدم nad 2-actyal aldhyed==bcetat //actyal dehydrogenas/هاي العمليه بتصير بالمايتوكندريا -nicin(b3)نقصان ال=caused by alchole intake or toxicity = hypoglycimia =no glycolysis + no gluconegensis

Answer 23

fembazole=inhibit alchole dehydrogenas=بمنع تسمم الكحول disulfrim= inhibitng actyal dehydrogenas =بعالج ادمان الكحول بعمل شعور زفت كل ماشربت

Answer 24

fembazole=inhibit alchole dehydrogenas=بمنع تسمم الكحول disulfrim= inhibitng actyal dehydrogenas =بعالج ادمان الكحول بعمل شعور زفت كل ماشربت

Answer 25

1-carbemyol phosphat synthasis = RATE limting step 5- step 5 = ump synthasis =useing PRPP from ribose cycle convert ortic acide to ump impaird in ortic acidico uria

Answer 26

imparmnt useing PRPP as co factor imperment of step 5 of pyramdin synthasis

Answer 27

lefenoooiamide== inhibts dihydroooortet dehydrogenas methotrooooxate+tri-sux= inhibit dihydroortet reductase hydRoxy uRia =Ribonuclutide Reductase flurourcil== inhibts ump=tmp= by inhibiting thymdylat synthase بمنع اعطاء يورسل للثايمن

Answer 28

lefenoooiamide== inhibts dihydroooortet dehydrogenas methotrooooxate+tri-sux= inhibit dihydroortet reductase hydRoxy uRia =Ribonuclutide Reductase flurourcil== inhibts ump=tmp= by inhibiting thymdylat synthase بمنع اعطاء يورسل للثايمن

Answer 29

1-prpp synthatase -first step

Answer 30

1-myclophenlate =inhibts imp converting to gmp=by inhibtion inosin monophosphat dehydrogenase 2- aztheroprin =inhibts all the pathway

Answer 31

blue stibbling =علامه غير خاصه تظهر في عدة امراض الدم ومنها التسمم بالرصاص blue ring=علامه خاصه فقط بالsifroblastic aniemia

Answer 32

صيدلية مهدئات بتبيع p اسمها cdk ال tp53+p21 بكسرهاا الRBبضل شغال =RB مدامه شغال مافي انقسام خلوي growth factor=cyclin=cyclin-cdk= inhibit RB(بريك) in g1 of cell cycleb اختصار RB=prevent deviasion by increasing tumer suprresor=((hypo phsphalration)) PB= decreasing growth factor =by phosphalryation of cdk cyclin complex

Answer 33

g1الي درسناه growth or go dievi= G0 خطوه الخلايا العصبيه والعضلات بضلو فيها s dna sunthasis g2 duplication of protien+dna m=cytokinas relase+itosis انواع الخلايا خلايا دائما بال g1c الجهاز الهضمي+خلايا دائما بالg0 زي الاعصاب + خلايا بين g1+0 زي الكبد

Answer 34

ser(hepato+adrenal)=remove toxin+make steroied +laste step of glycolysis +gluconew +noribosome rer(plasma cell+gi)=Site of synthesis of secretory (exported) proteins+ Nissl bodies (RER in neurons)—synthesize peptide neurotransmitters for secretion+ Free ribosomes—unattached to any membrane; site of synthesis of cytosolic, peroxisomal, and mitochondrial proteins. glgi=mdifing +disterpution of protiens modifing? -modifying N-oligosaccharides on asparagine - O-oligosaccharides on serine and threonine, and adding mannose-6-phosphate to proteins for lysosomal and other proteins.

Answer 35

II)—inherited lysosomal storage disorderلايسوسوزم مافيه انزيم (autosomal recessive); defect in N-acetylglucosaminyl-1-phosphotransferase failure of the Golgi to phosphorylate mannose residues ( mannose-6-phosphate) on glycoproteins enzymes secreted extracellularly rather than delivered to lysosomes lysosomes deficient in digestive enzymes buildup of cellular debris in lysosomes (inclusion bodie نفس اعراض هنتر بس اعراض اكثر Results in coarse facial features, gingival hyperplasia, corneal clouding, restricted joint movements, claw hand deformities, kyphoscoliosis, and plasma levels of lysosomal enzymes. Symptoms similar to but more severe than Hurler syndrome. Often fatal in childhood.

Answer 36

-اكسدت دهون طويله b -اكسدت دهون متفرعه الفا -اكسدت الكحول والاماينو اسيد Synthesis of bile acids and plasmalogens (important membrane phospholipid, especially in white matter of brain)

Answer 37

1-zellweger syndrom pex gen mutation? no peroxisome synthasis= fatt oxi =fat accumilation= hepatomegaly+cns symp 2-Refsum disease? disorder of α-oxidation (branch chain) buildup of phytanic acid due to inability to degrade it. Scaly skin, ataxia, cataracts/night blindness, shortening of 4th toe, epiphyseal dysplasia. Treatment: diet, plasmapheresis. 3- Adrenoleukodystrophy—X-linked β-oxidation due to mutation in ABCD1 gene VLCFA buildup in adrenal glands, white (leuko) matter of brain, testes. Progressive disease that can lead to adrenal gland crisis, progressive loss of neurologic function, death.

Answer 38

اي اشي عليه upiqintin بكسره neurodegenerative diseases.+mch1 respons defect

Answer 39

micro=actin + myosin intermediate= maintain cell structer macro= كل شي= devision+ cilia+fllagella= Drugs that act on microtubules (microtubules get constructed very terribly): Mebendazole (antihelminthic) Griseofulvin (antifungal) Colchicine (antigout) Vinca alkaloids (anticancer) Taxanes (anticancer)

Answer 40

موجودات عالmacro tuble kinin=attak =antegrade =neg to pos dynin=retrograd= pos to neg= tatani pilo+herpes +raipase=Primary ciliary dyskinesia=Dynein arm defect immotile cilia dysfunctional ciliated epithelia. Most common type is Kartagener syndrome بتبطل تقدر تخلف =Lab findings: nasal nitric oxide (used as screening test)ً

Answer 41

SCAB Type I - Skeleton+ late wond repair =osteogensis imperfecta type II - Cartilage =cartwolage Type III - Arteries =EhlersDanlos syndrome (threE D). Type IV - Basement membrane= under the floor (basement membrane). Defective in Alport syndrome; targeted by autoantibodies in Goodpasture syndrome. Myofibroblasts are responsible for secretion (proliferative stage) and wound contraction

Answer 42

1-procollgen=collgen alpha chain= adding glycin to prolin or lysin=ثلثه قلايسن 2- hydroxilation of prolin +lysin=يعني اضافهoh=needs vit c= scurvay diseas 3-glycolysation of lysin residual=يعني اضافه سكر للlysin=forming alpha helical shape=osteogensis imperfecta 4-ًexocytosis=cut the ends =to be procollgen= اسمهtopocollgen 5-alligin to assymble 6-cross linkedg = lysin hydrolxys bond

Answer 43

1- osteogensis imperfecta step 3 defect adding glucose to lysin=collgen type 1=Multiple fractures and bone deformitie +Blue sclerae B due to the translucent connective tissue over choroidal veins+((hearing loss +tooth abnormality)) 2-scurvey step 2 hydrolysiation of prolin + lysin add oh 3- eshelr syndrom 4 type -1 hyper mobility -2 cassical joint + skin=type 5cola2 ,1 -3 vassculer coolgen type3 cola 3a hyperextensible skin A , hypermobile joints B , and tendency to bleed (easy bruising) +May be associated with joint dislocation, berry and aortic aneurysms, organ rupture.

Answer 44

connective tissue disease caused by impaired copper absorption and transport due to defective Menkes protein ATP7A (Absent copper), vs ATP7B in Wilson disease (copper Buildup). -Leads to defcect in activity of lysyl oxidase (copper is a necessary cofactor) =no coolgen cross link step 7 اخر خطوه -symptom:defective collagen cross-linking. Results in brittle, “kinky” hair, growth and developmental delay, hypotonia, risk of cerebral aneurysms

Answer 45

الفرق بينه وبين الcollgen انو هذا non hydroxylated =Cross-linking occurs extracellularly via lysyl oxidase and gives elastin its elastic properties. مطاطيه للشرايين والlungs copd= high elastas coause no antitrepsin =تكسير اليلاستين =Tropoelastin with fibrillin scaffolding.=مكونات الفايبر =Marfan syndrom=FBN1 gene mutation on chromosome 15 (fifteen) results in defective fibrillin-1, a glycoprotein that forms a sheath around elastin and sequesters TGF-β. =Homocystinuria—most commonly due to cystathionine synthase deficiency leading to homocysteine buildup. Presentation similar to Marfan syndrome with pectus deformity

Answer 46

DNA methylation= mute dna expression =aging, carcinogenesis, genomic imprinting, transposable element repression, and X chromosome inactivation (lyonization) عدم وجود methylation بنشوفه في Fragile X syndrome histone methylation = mute dna expression =Lysine and arginine residues of histones can be methylate histone acyle=acyive expression=Thyroid hormone synthesis is altered by acetylation of thyroid hormone receptor. histone deacyle=deactive=Huntington disease

Answer 47

1-Cladribine, pentostatin=inhbits ADA= inhibits ((adenosin deaminase)) if deffency =scid 2-Allopurinol Febuxostat =XO 3-rasburicase= Urate oxidase=inhibits converts uric acid to Allantoin 4-Lesch-Nyhan syndrome=hgprt deff

Answer 48

1-Adenosine deaminase deficiency=decreasing ribonucleotide reductase activity= decreasing DNA precursors in cells =decreasing lymphocytes. ==scid=sever compaind immune deffency 2-Lesch-Nyhan syndrome= مش موجود الhgprt which is enzyem re use imp gmp=if deffect no gmp + no imp = increasing purin synthasis = increasing degradation of purin = uric acid acuumulation in joint muscle cns + gout +macrocytosis . tretmant =inhbits hypoxanthin oxi =Allopurinol + Febuxostat

Answer 49

Most amino acids are coded by multiple codons.==Exceptions: methionine (AUG) and tryptophan (UGG) encoded by only 1 codon. -code = sequance of nuclotieds=found in mRNA -anti codon = found in tRNA =عشان يقراء ويعرف شو يجيب -wobble hypothysis = each sequence of nuclotied first 2 nuclotied = for attachment the last part= يحدد نوع الAA

Answer 50

-helicase=sepreats the D DNA from each other=deffecincy in bloom syndrom (blm gene mutation) -topoisomerse =works forword of helicas to un wind complecated DNA = inhibited in eukariotic by irinotecan/topotecan -primas=makes complematry RNA in tatabox to start with. =البناء يكون من3 ل5: -dna poly 3= in prokariatic only = elongate leading + lagging strand= has 5-3 only activity only -dna poly1=in prokaritic only= elongate leading + lagging strand = has 3-5 for removal of rna primase and 5-3 exonucloes activity -tolemtase =makes taaagggaa =tag عشان يحمي الdna

Answer 51

-Double strand= 1-non-homologous end joining ==dna may be lost or translocated= ataxia telangiectasia. 2- homologues end join= using a complementary strand from intact=without loss of nucleotides.=BRCH1 +fanconi anemia -single strand repair = 1-Nucleotides excision repair=remove the group of nuclotieds then synthasis another =xeroderma pigmentosum 2-Base excision repair=remove one base then synthasis another =repair of spontaneous/toxic deamination. 3- Mismatch repair=only one nuclotied wrong remove 10 nuclotied then add new seen in polymares activity= Lynch syndrome (hereditary nonpolyposis colorectal cancer )

Answer 52

Degree of change: silent << missense < nonsense < frameshift . Types of single nucleotide (point) mutations=repaired by DNA polymerase and DNA ligase • Transition—purine to purine or pyrimidine to pyrimidine • Transversion—purine to pyrimidine او العكس

Answer 53

Single nucleotide substitutions? -silent=Codes for same (synonymous) amino acid; -senc=Results in changed amino acid =((sickl cell diseas)) -nonsence=Results in early stop codon nonsense! (UGA, UAA, UAG) other? Frameshift mutationبعمل امراض غاليه ونادره وحلوه=Deletion or insertion of any number of nucleotides=Duchenne muscular dystrophy, Tay-Sachs disease, cystic fibrosis. Splice site mutation=Retained intron in mRNA protein with impaired or altered function=cancers, dementia, epilepsy, some types of β-thalassemia, Gaucher disease, Marfan syndrome.

Answer 54

Single nucleotide substitutions? -senc=Results in changed amino acid =((sickl cell diseas)) -nonsence=Results in early stop codon nonsense! (UGA, UAA, UAG) other? Frameshift mutationبعمل امراض غاليه ونادره وحلوه=Duchenne muscular dystrophy, Tay-Sachs disease, cystic fibrosis. Splice site mutation=cancers, dementia, epilepsy, some types of β-thalassemia, Gaucher disease, Marfan syndrome.

Answer 55

-Eukaryotes 1-RNA polymerase I makes rRNA=the most common (rampant) type; present only in nucleolus. 2-RNA polymerase II makes mRNA=massive), microRNA (miRNA), and small nuclear RNA (snRNA). 3-RNA polymerase III makes 5S rRNA, tRNA (tiny -Prokaryotes 1 RNA polymerase (multisubunit complex) makes all 3 kinds of RNA

Answer 56

Dactinomycin inhibits RNA polymerase in both prokaryotes and eukaryotes. -Eukaryotes-رمت 1-RNA polymerase I makes rRNA=Dactinomycin 2-RNA polymerase II makes mRNA=Dactinomycin 3-RNA polymerase III makes 5S rRNA, tRNA (tiny=((Dactinomycin))α-amanitin, found in Amanita phalloides (death cap mushrooms), inhibits RNA polymerase II. Causes dysentery and severe hepatotoxicity if ingested. -Prokaryotes 1 RNA polymerase (multisubunit complex) makes all 3 kinds of RNA=(( Dactinomycin))inhibeted by (rifampin,

Answer 57

Ataxia-telangiectasia is characterized by DNA hypersensitivity to ionizing radiation. In xeroderma pigmentosum, DNA is hypersensitive to UV radiation, causing premature skin aging and increased risk of skin cancer (malignant melanoma and squamous cell carcinoma). Fanconi anemia is caused by hypersensitivity of DNA to cross-linking agents. Bloom syndrome is characterized by generalized chromosomal instability. Increased susceptibility to neoplasms is present. Hereditary nonpolyposis colorectal cancer (HNPCC) occurs due to a defect in DNA mismatch-repair enzymes. It leads to increased susceptibility to colon cancer.

Answer 58

اختصارهم :اكيد vit E= anti-oxidant protact rbc and nurons=demylenatic of dorsi colmuen+spincebler tract=ataxia also cause+hemoltic animia

Answer 59

anatomy=striatum cosist of putin+cudat nucli function=striatum (مصنع اقفال)giva only gaba (قفلل) for gpe +gpi direct pathway=give gaba قفل for gpi =محل الاقفال=حركه gpi=يضع اقفال للمحرك فقط(thalamus) gbe=يضع قفل للمطرقه (stn) no one broke gpi = التي تكسر gpi indirect pathway=give gaba for gbe بعطي قفل لمحل الاقفال = no one stop gpi = no movement

Answer 60

- Huntington disease=(CAG)=Caudate has decreas ACh and GARA - Myotonic dystrophy= CTG=Cataracts, Toupee (early balding in males),Gonadal atrophe in males, reduced fertility in femal -Fragile X syndrome=CCG=Gonadal atrophe in males, reduced fertility in +Friedreich staxia =GAA=Chin (protruding), Giant Gonads

biochem Flashcards

(86 cards)