| 7564168076 | Other name of B12 | Cobalamin | | 0 |
| 7564171386 | Moieties of cobalamin | Corrin ring (4 bonded pyrrole rings with cobalt in the middle. 4 rings make the shape)
Cobalt (in the center of four pyyrole rings comprising the corrin structure) | | 1 |
| 7564197257 | What are the two synthetic forms of cyanocobalamin ? | -Cyanide in synthetic pill form | | 2 |
| 7564208572 | What makes up members of the family called cobalamins? | Corrin ring and Cobalt | | 3 |
| 7564223132 | What are the vitamers of B12? | These have cobalimin in their name but carry different groups:
-Nitritocobalamin (carries NO group)
-Cyanocobalamin (carries Cn aka cyanide group which is the synthetic)
-Hydroxocobalamin (carries OH group)
-Aquocobalamin or hydrocobalamin (H2O group) carries water
*some of these vitamers can be used to make 2 coenzymes | | 4 |
| 7564245413 | Coenzymes of B12: | Two coenzyme forms are taken from some of the vitamers and converted into coenzyme form
-*Methylcobalamin (CH3 group)
reminder: cobalamin+CH3___>*methylcobalamin
*5-methylTHF
-*Adenosylcobalamin | | 5 |
| 7564323928 | How can we take one of the vitamers and covert it to one of the coenzymes? | -Hydroxocobalamin+H+ + ATP____>*adenosylcobalamin
Hydro modified to get one of the coenzymes
-Hydroxocobalamin+CH3___>*methylcobalamin
-Cyanocobalamin___> *methylcobalamin or *adenosylcobalamin
two coenzymes form made from cyanocobalamin, shows interconversion to get coenzymes | | 6 |
| 7564360606 | Sources of cobalamin | Plant sources: cant make it
ONLY FROM MICROBIAL SYNTHESIS/FORTIFICATION
Animal sources: cant make it
*Can make some from our colon because we have microbes that can make it
If we get it from chicken, beef, fish, soy, eggs it's because the microbes in the animals make the vitamin, the animals themself did not have them
Plants can be fortified with B12 as well as cereals | | 7 |
| 7564382599 | Types of supplements | Cyanocobalamin and Hydroxocobalamin | | 8 |
| 7564391627 | B12 in foods? | Really tightly bound to protein. High affinity, vitamin tightly bound to food and there needs to be a way to liberate the vitamin in stomach from the food protein. HCL and Pepsin help by taking it apart and we get free vitamin in stomach, otherwise we wouldn't get it, now you have free vitamin B12 in the stomach but it needs to be bound to a protein carrier in stomach (aka R protein: trans cobalamin 1)
cobalamin+ food protein___>cobalamin-protein complex(in food)
cobalamin-protein complex__>free cobalamin + protein HCL and pepsin | | 9 |
| 7564426601 | Mouth | Saliva contains carrier proteins that attach to B12 in the stomach to protect B12 from destruction by stomach acids | | 10 |
| 7564436904 | True or False
No trouble processing from B12 from pill | True | | 11 |
| 7564438955 | Duodenum | B12 attaches to Intrinsic Factor (IF) | | 12 |
| 7564487287 | Transcobalamin 1 and Intrinsic Factor (IF) | B12-R protein complex___>free B12 + AA+peptides
pancreatic proteases (digest protein, hydrolize tans co 1)
1. In stomach, it is released and vitamin B12 gets attached to transcobalamin 1, this is how it gets out of stomach and into duodenum. Transcobalin 1 protect B12 so microbes can't get it
2. In duodenum, transcobalamin 1 gets hydrolyzed (absorbed) into AA. Leaves B12 without carrier. Cobalamin released from carrier in duodenom and now it is alone but we cant leave it alone.
Intrinsic Factor:
3. Once Transcobolin 1 digested, it's left on its own, that's when it gets picked up in duodenum. Has to travel to ileum
free B12+IF___>B12-IF complex
B12 has to constantly be bound to something (ex: IF) | | 13 |
| 7564606740 | Implications for persons with genetic mutations | Have trouble getting B12 from stomach to ileum.
Ex: Genetic problems | | 14 |
| 7564614955 | Where is IF synthesized? | ????????????????????????? | | 15 |
| 7564617513 | What type of molecule is IF? | Glycoprotein (has carbohydrates in its structure) | | 16 |
| 7564625759 | Where is the site of interaction of IF with B12? | Duodenum | | 17 |
| 7564636690 | Factors that can interfere with cobalamin digestion and travel: | If you don't produce enough pepsin or HCL in stomach, you'll have trouble releasing B12
If producing too much acid you can denature IF. Proteins that don't do well in a lot of acid could destroy IF or cobalamin 1. Insufficient production will interfere with travel from stomach. | | 18 |
| 7564648847 | Absorption of cobalamin | Ileum | | 19 |
| 7564651248 | Primary site of cobalamin absorption | ilem | | 20 |
| 7564653898 | Role and composition of cuban receptor | When the vitamin reaches ileum, it's still attached to IF, when B12 complex reaches ileum, forms physical attachment between brush border cells of ileum because that's how absorption happens. There is a physical attachment between the vitamin complex and attachment cells. They find receptor for receiving IF B12 complex. Located outside of cell like a lock. Receptor is a lock made to fit to one another. B12 complex is the key. B12 complex gets through, the receptor is called cubam | | 21 |
| 7564772040 | What does cubam stand for | Cubilin
Aminoless
Megalin=Cuban receptor on brush boarder of ileum | | 22 |
| 7564784800 | What is the name of the receptor that accepts IF B12 complex at the brush border of the illeum | cubam | | 23 |
| 7564786719 | Which is a part of the cubilin receptor | Amnionless | | 24 |
| 7564813462 | If you get B12 from food, we use______________- | active transport | | 25 |
| 7564830577 | Absorptive mechanism with physiological intakes | Damage could be mutation or damage of gene and person could experience malabsorption | | 26 |
| 7564836040 | Absorptive mechanism with pharmacological intakes - | B12 malabsorption could happen if person has celiac or chromes disease or brush border get or vili damage=inadequate absorption | | 27 |
| 7564853669 | Factors that can decrease B12 absorption at the distal ileum = | It can't be absorbed at ileum. Condition called atrophic gastritus - certain cells of stomach get destroyed, antibodies destroying
If your'e not eating enough B12 you won't absorb enough
Removing distal part of ileum where absorption takes place | | 28 |
| 7564867841 | Atrophic Gastritus- | Certain stomach cells destroyed and inflammed. Autommune condition, antibodies destroy partial cells of stomach. Less travel and absorption, leads to decrease reduction of intrinsic factor less B12=Pernicious Anemia | | 29 |
| 7564890320 | Zoolinger Elsen- | LOOK IN BOOK
make too much stomach acid | | 30 |
| 7564904408 | Transporters inside the enterocytes | -ABC drug transporter
-Transporter II transporter
Enterocytes always have to keep some. Some B12 stay in enterocyte, some carry to basal lateral membrane to get into blood. | | 31 |
| 7564909951 | ABC drug transporter | Inside enterocyte, picks up vitamin and takes to basal lateral membrane so B12 can get out | | 32 |
| 7564913640 | Transcobalamin II transporter- | Located at basal lateral membrane, backdoor. Takes vitamin into blood
First stop liver | | 33 |
| 7564935508 | What mechanism does the body use to protect you from a B12 deficiency ? | Recycling
one way nature has of protecting from B12 deficiency
Absorb B12 from food or pills
Some vitamin when get into liver are dumped into bile and goes to galbladder, when vitamin reaches small intestine it meets up with intrinsic factor and goes to ilieum and is recycled | | 34 |
| 7564956312 | If you get Vitamin B12 from food- | we use active transport for IF B12 complex to get in cell | | 35 |
| 7564957461 | Glove- | endosome, Vitamin IF released from endosome end up at lysosome, digested and B12 released | | 36 |
| 7564977538 | If you consume vitamin from normal doses from food___- | mechanism of absorption is endocytoses
if consumed in big doses, happens with passive diffusion | | 37 |
| 7564982873 | Two most abundant vitamers of B12 in portal blood | the coenzyme forms
-Adenosylcobalamin
-Methylcobalamin
These travel through the blood and are absorbed and get i blood as coenzyme form, food form | | 38 |
| 7565010398 | Other forms of B12 in portal blood- | Hydroxl and cyamical, synthetic forms that end up in blood | | 39 |
| 7565032575 | Protein carriers for B12 in portal blood | needs carrier
TCI
TCII
TCIII | | 40 |
| 7565034906 | TCII- | Takes B12 in blood, carries 20% of vitamin in blood. Located on basal lateral membrane, gives up some share to TCI
a protein | | 41 |
| 7565040358 | TCI- | found in stomach and blood, 80% carries vitamin through blood, carries more than TCII
a protein | | 42 |
| 7565044221 | TCIII | special case, distributes B12 from liver to tissue in need, send some B12 out of liver to needy areas like a first responder | | 43 |
| 7565064871 | TCII receptors on plasma cell membranes- | Receptors for TC1 & II. Carriers are key. Receptors are lock
Outer membrance makes glove around TCI or II and bring in vitamin, endosome makes its way over lysosomes, TCI and II destroyed releasing vitamin then vitamin can go out. Once protein released in cytosome it gets escorted to wherever it needs to go like mitochondria or nucleus | | 44 |
| 7565085501 | What happens to a persons B12 status if there were a mutation in the gene that encodes for the TCII carrier protein | Less carriers available
Things won't go well unless you bypass small intestine with injections, bypass GI tract to blood | | 45 |
| 7565110850 | What is a possible health consequence of low blood B12 concentrations? | High homocysteine levels, CVD risk and stroke | | 46 |
| 7565113627 | B12 storage in tissues and organs | Body does not want to give it up, we dont store a lot but we store in liver, muscle, kidney, brain, spleen, heart | | 47 |
| 7565127317 | Primary B12 vitamer in body tissues and organs | Adenosylcobalamin (the coenzyme form) | | 48 |
| 7565135295 | Primary B12 vitamer in blood | Methylcobalamin | | 49 |
| 7565196149 | Metabolism or Cobalamin:
Interconversion of B12 vitamers in body cells | -Hydroxocobalamin+CH3>*methylcobalamin
(pill form)
-Hydroxocobalamin+H+ + ATP> *adenosylcobalamin
need ATP because its donor of adenosyl group for adenosylcobalamin
ATP was donor
-cyanocobalamin>aquocobalamin
decyanase
-cyanocobalamin > hydroxocobalamin+CN
decyanase
hydroxo can give methyl or adenosyl
cyano and hydroxo are 2 pill forms | | 50 |
| 7565280588 | Methyllcobalamin and (Met) Metabolism
The Cycle
*methylcobalamin and the coenzyme *5-methyl THF of folate catalyze the reactions that lower blood homocysteine levels and regenerate MET from homocyteine | 1. B12 coenzyme
2. Folate coenzyme | | 51 |
| 7565348312 | Roles of folate and B12 in regenerating Methionine from homocysteine | Step 1: Formation of homocysteine from Met
SAM can leave here because the cycle keeps myelin sheath healthy, dontes methyl group
Step 2: Formation of s-adenosyl homocysteine (SAH)
Step 3: Formation of homocysteine
Step 4: Regeneration of methionine from homocysteine
Homocysteine+ *methylcobalamin>Met+cobalamin
Methionine synthase | | 52 |
| 7565408672 | a B12 deficiency could lead to | Met since this vitamin is needed to regenerate Met from homocysteine | | 53 |
| 7565425992 | *Adenosylcobalamin and Succinyl-CoA Synthesis | Part of TCA cycle
Won't be able to get as much energy from macronutrients
If we don't have enough of we can't make enough Adenosylcobalamin Succinyl CoA and TCA cycle will show and won't be able to get as much nutrients | | 54 |
| 7565489295 | Reactions that generate succinyl-CoA | Step 1: Methionine or Isoleucine or Thrionine> propionyl-CoA
Step 2: propionyl-CoA>methylmalonyl-CoA
Step 3: methylmalonyl-CoA>succinyl-CoA
methylmalonyl-CoA mutase and * adenosylcobalamin
P
M
S
requires adenosyclcobalin | | 55 |
| 7566100120 | what compounds would accumulate in the blood of someone with B12 deficiency or a mutation in the gene that codes for methylmalonyl-CoA mutase | Rxn wont move well, we wont make as much succinyl CoA and low on energy
methylmalonyl-CoA___>methylmalonic acid
a consequence is we will accumulate these in blood and spill out in urine, not suppose to excrete a lot of meth acid
methylmalonic acid is a derriviate of methylmalonyl CoA and builds up high and spills in urine | | 56 |
| 7566127951 | Treatment of the genertic disorder methylmalonic acidemia | if you take high doses it can be useful and faster and better. People can absorb it better at the ileum | | 57 |
| 7566132923 | Unsubstainable claims for uses of B12 in pharmacological doses | Help lose weight, If high doses taken meth CoA will work faster and better so more Suc CoA made and TCA cycle works better. People can absorb by passive diffusion with pills | | 58 |
| 7566139041 | The folate trap in the liver | Folate gets stuck in liver as 5 methyl THF
If you dont have enough B12, folate gets trapped, can't make as much as other coenzymes. Less material to make other CoA. Need B12 to take methyl away from SMTHF, loses methyl to become THF=vitamin dependent of eachother | | 59 |
| 7566152386 | Primary route of B12 excretion | Does not get excreted much
Bile, but we can get most back, recycled, 75 percent gets reabsorbed | | 60 |
| 7566179706 | reabsorption of B12 excreted in bile | lose some but get back a lot | | 61 |
| 7566182220 | Frequency of occurrence of B12 toxicity | rare | | 62 |
| 7566185472 | Has UL been set for B12 | no because toxicity is rare | | 63 |
| 7566186839 | Cobalamin Deficiency | 2 categories:
1. Neurological - Brain and CNS. Symptoms because of myelin sheath, maintained by compounds like SAM to donate methyl groups to mylein sheath to maintain it
2. Hemotological - anemia. macrocytic and megoloblastic. person given folate but balance messed up
tingling numbness and lack of coordination | | 64 |
| 7566203038 | Primary cause of B12 deficiency in US | Absorption problem, small pills, easy to take but hard to absorb | | 65 |
| 7566207047 | Name of the B12 deficiency condition and its symptom | Pern anemia, refers to what happened, what was cause of the deficiency?
pern as cause of anemia is rare | | 66 |
| 7566210769 | stages of B12 deficiency and their features | blood level can be normal but tissues down
1. Initial stage- 1st blood levels go down but not always good indicators cant always tell whats happening in tissues
2. Second stage-
3. Third Stage- Homocystein high meth acid high. Folate traked. If folate and B12 deficient thats when you get damage to RBC. If you don't have B12 can't regenerate methronine, homo stays high meth low
w/o meth inadequate sam
whole cycle messed up. Sam and meth low | | 67 |
| 7566231271 | Urinary methylmalonic acid concentration | Suppose to be small
FIND THE NUMBER
goes up in urine in B12 def | | 68 |
| 7566233276 | the schilling test | use radiation for B12 measure the amount in the urine
FIND THE POINT AND WHAT THEY LOOK FOR | | 69 |
