Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

NHM 561 > Vitamin B12 (4 questions) > Flashcards

Vitamin B12 (4 questions) Flashcards

(48 cards)

Start Studying
1
Q

What are the coenzyme forms of Vitamin B12?

A

Methylcobalamin

5-deoxyadenoslycobalamin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Food Sources of B12

A
  1. Clams
  2. Liver
  3. Fortified yeasts
    …Seafood, Fish (salmon, trout, tuna, haddock)
    …Beef
    …Dairy

Not naturally found in plant-based foods (these are fortified)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

R BINDER

A

Secreted into saliva into the mouth

Low pH environment in the stomach favors the binding of cobalamin to R Binder

No action until it binds with cobalamin into the stomach, after pepsin frees B12 from food

Once in the duodenum, biliary and pancreatic secretions degrade R Binder and cobalamin binds with IF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

PEPSIN

A

Gastric pepsin releases the food-bound cobalamin in the stomach by breaking down the protein and any food that B12 is a part of

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

B12 Absorption - - What is in the stomach?

A

Mix of:

-Cobalamin (free form due to pepsin)

-R-Binder

-IF (secreted by parietal cells)

-B12-R Binder Complex (due to HCl acid)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

The low pH of the stomach (caused by HCl acid) favors what?

A

FAVORS the binding of B12 to R-Binder in the stomach

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

IF

A

Secreted in the stomach by the parietal cells

It is along for the ride, until it reaches the duodenum, and will bind to cobalamin, which will move to the ileum

It can bind to cobalamin because biliary and pancreatic secretions degrade R-Binder

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

B12 Absorption - - What happens in the duodenum?

A

Biliary and pancreatic secretions degrade R-Binder protein, allowing cobalamin to bind to IF, and move to the ileum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

IF-B12 Cobalamin Complex

A

Taken up directly into the ileal mucosal cells, through endocytosis, and brought into the cytoplasm, and makes its way to the lysosome

It is split in the lysosome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Where does cobalamin-IF complex split?

A

In the lysosome of the ileal mucosal cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

B12 Absorption - - What happens in the lysosome?

A

IF-Cobalamin complex is split

Cobalamin is bound to TCII (transcobalamin II; a binding protein)

and exits the enterocyte, and enters systemic circulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How much B12 can be passively absorbed?

A

About 2%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

At what oral dose does B12 absorption decrease? Why?

A

Above 0.25 micrograms

The cubilin-amnionless receptors can become saturated, and excess B12 is secreted in the urine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

(T/F) B12 is excreted in bile. Explain.

A

TRUE

Bile is synthesized in the liver, taken to the GB, then secreted into the S.I.

a) Bile helps w/ digestion and absorption of lipids
b) Some B12 are part of bile acids and bile salts

Bile can be reabsorbed in the S.I. (including the B12 w/in the bile). This process is the exact same in the ileum. AKA IF is required.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Enterohepatic circulation

A

B12 is excreted in bile but can bind IF in the duodenum and be reabsorbed in the ileum.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

TCII

A

Transcobalamin II; binding protein, that binds to cobalamin in the lysosome and then goes to portal circulation, then systemic circulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Portal Circulation

A

The circulation of nutrient-rich blood between the gut and the liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the 2 receptors for cobalamin-TCII complex?

(on peripheral tissues in systemic circulation)

A
  1. Holo-TCII Receptor
  2. Megalin

Expressed on peripheral tissues

Responsible for bringing the cobalamin-TCII complex into the cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Once in the cytoplasm (of peripheral tissues), cobalamin is converted to what?

A

Methylcobalamin (coenzyme form)

To be used for homocysteine metabolism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

In the mitochondria (of peripheral tissues), cobalamin is converted to what?

Study These Flashcards
A

5-deoxyadenosylcobalamin (coenzyme form)

It is used for propionyl-Coa metabolism

21
Q

In a healthy adult, how much cobalamin is stored?

Study These Flashcards
A

About 2,500 micrograms (2-3 mg)

22
Q

What is the distribution and where is cobalamin stored

Study These Flashcards
A

50% in the LIVER

30% in MUSCLE

20% in pituitary glands, bones, kidney, heart, brain, spleen

23
Q

(T/F) A lot of B12 is lost daily.

Study These Flashcards
A

FALSE - only about 1 microgram a day (very, very low) due to B12 recycling via enterohepatic recirculation

24
Q

How long would it take to see clinical signs of deficiency, in a normal healthy adult?

Study These Flashcards
A

About 2-5 years

Resulting from a complete loss of IF

Seen in the elderly population

25
What is the primary function of methylcobalamin?
Needed for methionine and homocysteine metabolism
26
Methionine Synthase
This enzyme binds cobalamin Takes a methyl group from 5-methyltetrahydrofolate (THF) and transfer it to cobalamin, becoming methylcobalamin Thus converting 5-methylTHF ---> THF
27
How is homocysteine created?
Methylcobalamin still attached to methionine synthase is going to transfer that methyl group to homocysteine This creates/synthesizes methionine
28
Methionine
Very important AA because it is converted to SAM (S-adenosylmethionine)
29
S-adenosylmethionine
SAM Able to transfer its methyl group to DNA and other proteins -these thousands of proteins are activated when they receive a methyl group -this creates SAH
30
S-adenosylhomocysteine
SAH Generated when SAM transfers methyl group to DNA and other proteins SAH is converted to homocysteine
31
Homocysteine
"Bad Guy" Higher homocysteine is associated with increased risk of CVD, including venous thrombosis, atherosclerosis, high BP, CAD, and stroke --aka needs to be kept in check High homocysteine levels are a good indicator if someone has low B12, or folate, or even B6
32
If more methionine is not needed, what happens?
Homocysteine can be metabolized --------------------------------> Cysathionine Cystathionine Synthase (PLP dependent; coE of B6)
33
Explain how homocysteine can be converted back to methionine
The reaction requires the methyl group from folate to be transferred over to cobalamin, creating methylcobalamin. Then methylcobalamin is going to give its methyl group to homocysteine, therefore synthesizing methionine
34
What is the function of coE form 5-deoxyadenosylcobalamin?
It is going to act as a cofactor for the enzyme, methylmalonyl-CoA mutase -It is the sole function of this coE.
35
Propionyl-CoA
a 3-carbon FA that comes from the odd-chain FA metabolism (aka: the 3 carbons leftover from beta-oxidation) OR it can come from BCAA metabolism
36
Why is MMA bad?
MMA = D-methylmalonic acid associated with destabilizing myelin, and promoting the formation of deformed or highly destabilized myelin
37
Myelin
the insulating layer or that sheath that covers nerve cells helps to transmit the electric impulses (messages) through the nerve, from one nerve cell to another
38
MMA build-up is going to potentially cause....what?
Nerve damage; reduced cognition Been shown that it can inhibit complex II of the ETC, and therefore can cause problems with oxidative phosphorylation (which can result in not having enough biosynthesis of ATP)
39
High blood levels of MMA and low B12 markers, would indicate what?
CoE. B12 deficiency of 5-deoxyadenosylcobalamin
40
Megaloblastic Anemia
Frank B12 deficiency appears as multi-lobular/hyper-segmented neutrophils and oval shaped RBCs
41
What population is at increased risk of B12 deficiency? Why?
Elderly Gastritis (acute or chronic) ---Autoimmune gastritis ---H. Pylori infection Not from lower intakes of B12 except for long-term vegans
42
Autoimmune Gastritis
Antibodiesin the stomach that attack parietal cells Major inflammation prevents those cells from secreting HCl acid, pepsin, and other digestive enzymes
43
H. Pylori infection
Bacteria that invade the stomach lining, causing inflammation, blocking secretion of those enzymes that are needed to lower the pH and breakdown food
44
What are secondary deficiency clinical manifestations of B12?
Neurological changes (dementia, confusion symptoms) Due to build-up of MMA and destabilization of myelin
45
Multi-lobular and oval shaped RBCs indicate, what?
Megaloblastic anemia (B12 deficiency)
46
How does roux-en-Y gastric bypass cause B12 deficiency?
Combination of decreased intake Lack of IF Reduced gastric acid Impaired absorption due to bypass of proximal S.I.
47
What are other subclinical cobalamin deficiency symptoms or clinical manifestations?
Any 2 or more: ---Increased MMA ---Increased plasma homocysteine ---Decreased [cobalamin] ---Decreased [holotranscobalamin II] Individuals s/p RYGB are at increased risk for these. Not all will be present with frank megaloblastic anemia
48
How is B12 assessed?
No gold standard Will run a panel for all water-soluble vitamins Use SERUM COBALAMIN (~200-250 ng/L for deficiency) --Holo-TC II assay --Serum MMA (indicates B12 deficiency ALONE, if high) --Serum homocysteine (could be confounded by folate status) There is no official upper limit

NHM 561 (21 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions