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Ch-10 (water-soluble Vit)

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ahmed's version from 2016-08-17 03:42

Section

Question Answer
B2 (riboflavin) & FAD enzAll DH
B2 (riboflavin) & FAD usageTCA
B2 (riboflavin) & FAD def cuase-rare to be def solo. Usually with other defs
B2 (riboflavin) & FAD def sympt●corneal neurovascular pathy ●cheilosis or stomatitis (cracking lips borders) ●magenta colored tongue (hallmark)
B3 (niacin) enz & usage All DH Makes: NAD(H) & NADP(H) [TCA]
B3 (niacin) def cause & sympt-easily def by diet -pellagra: Dia, Demintia, Dermatitis, Death (4D)
B6 & PLP enz Aminotransferase (transaminase) δ-aminoLevuLinate synthase
B6 & PLP enz usage-Pr catabolism -amine detoxification in liver (amine causes lipolysis) (amine: strong base) -PLP synth Heme synth
B6 & PLP def causeshepatic damage = B6 def (OH, isoniazid therapy)
B6 & PLP def sympt sidroblastic anemia (B6 def PLP defno heme in RBC microcytic anemia & accumulation of unused heme) ●convulsions (due to ischemia to CNS) ●cheilosis or stomatitis (cracking lips borders)
B12 (cyano-cobalamin) enz Homocystine methyltransferase Methylmalonyl CoA mutase
B12 (cyano-cobalamin) enz usageUntraps folate from its stored (inactive) form (uses methionine; SAM) VOMIT / TCA
B12 (cyano-cobalamin) def causesalmost never def due to diet, but due to terminal ileum path: B overgrowth, resection 2ndry to Crohn, chronic panct (cuz then panc wouldn’t release its enz that are involved in B12 absr), D. latum inf. -vegans don’t experience its def.
B12 (cyano-cobalamin) pathsmegaloblastic Anemia (B12 def inactivated folate no DNA  macrocytic anemia) ●progressive peripheral neauropathy (no B12  no TCA  no ATP  Neurons damage)
Follic Acid (folate) enzThymidylate synthase
Biotin enzPyruvate CX Acetyl CoA CX Propionyl CoA CX
Biotin enz usageGluconeogenesis: building glc from scratch (between meals) FA synthesis VOMIT: Val, odd-carbon FA, Met, Ile, Thr. (its sis enz is about eating raw eggs)
Biotin source Raw eggs consumption
Biotin def symptfasting hypoglycemia: drop of glc in between meals (not directly after a meal) -Alopecia (hair loss), bowl infl, muscle pain (signs of energy loss - severe glc or FA loss)
Follic Acid (folate) enz usage Make THF (the active form of folic Acid)
Follic Acid (folate) essential for?-THF is essential for DNA synth (no ATP involvd)
Follic Acid (folate) MCC of defMCC of def: OH & preg. (body storage of it is suff for 3 months; 1 trimester)
Follic Acid (folate) def symptMegaloblastic (macrocytic) anemia: No DNA  no mature RBC they stay big in BM ●def in early preg spinal bifida (its adviced to intake lots of it pre-preg.) ●homocystinemia: causing DVT & As
vit C (ascorbate) enz & usagePolyl & lysyl HX Dopamine HX Collagen synth CAT synth
vit C (ascorbate) def cause-easily def from diet
vit C (ascorbate) iron relation?-transforms plants Fe3 to Fe2 in GIT lumen, which is absorbable
vit C (ascorbate)def symptscurvy: weak tissues, easy bruise, poor healing, bleeding gums, anemia inc bleeding time (also sign of vit K def).
collagen uses?-collagen is used to strengthen tissues & in clots
Pantothenic acid CoA enzFA synthase FA CoA synthase Pyruvate DH α-ketoglutarate DH
Pantothenic acid CoA enz usage?FA metabolisms PDH TCA
Pantothenic acid CoA def causes?-almost never def
Pantothenic acid CoA main funused to make all CoA
CX: require to work?A.B.C. (ATP, Biotin, Co2
TCAcrep cycle (ATP production) tri-CX acid
confabulationin denial. Pt believes strongly in the lies he says, cuz he can’t remember the truth, so it makes sense to him. He forgets the truth cuz OH causes neuronecrosis
Trp def causesNiacin def  Pellagra. (HARTNUP is pellagra that is caused by trp def. genetically, kidneys fail to retain filtered trp cuz its too small, resulting in huge trp loss  pellagra)
B1 (thiamine) enzPyruvate DH, α-ketoglutarate DH Transketolase Branched chain ketoAcid DH
B1 (thiamine) enz usagePyruvate + PDH = Acetyl CoA Acetyl CoA in TCA = Co2 + electrons HMP shunt Metabolism of Val, Leu, Ile
B1 (thiamine) cofactor dependancepyruvate & αketo: are dependent on 5 cofactors; B1 is one of them. Transketo; is dependent on only B1 (clinically: measure transketo levels to measure B1 def)
B1 (thiamine) pathogenesis of defOH interferes with B1 absr. No B1  no TCA no E’  no Na pump  inc IC Na (mostly neaurons & cardiocytes; cuz they use lots of TCA) swollen cells  necrosis & symptoms. -to suppl it: give B1 + glc
B1 (thiamine) def symptwernicke: ataxia & nystagmus ●korsakoff: psychosis & confabulation ●wet beri beri: HF inc cardiac output
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