Flashcards in Vitamin B12 Deck (32):
Immature RBC that sometimes increase in the circulation in response to anaemia (produced by bone marrow)
Low haemoglobin indicates?
What is required for normal erythropoeisis?
-iron, folate, B12
Macrocytosis? Potential cause?
Larger the normal RBC, can be caused my 'megoblastic anaemia'
What is required to absorb B12?
-normal acid secretion
-normal pancreatic secretion
- normal terminal ileal absorptive function *
How is B12 actually absorbed?
1) gastric acid/pepsin releases food-bound B12
2) R-binders (saliva & stomach) bind to B12 in the stomach
3) Pancreatic enzymes can then help release B12 from R-binders to allow for binding to IF in SI
4) B12 has to bind to IF for absorption by specialised receptors in the terminal ileum
If the B12 deficiency is a stomach issue, what is wrong?
Lack of IF due to pernicious anaemia, and autoimmune disease (ABs against IF and parietal cell)
- not enough IF to bind to B12, impaired absorbtion
If the B12 deficiency is a small intestinal issue, what is wrong?
Surgery to remove terminal ilem or Crohns disease (IBD).
-B12 binds to IF but isn't absorbed by SI
What is the 'schillings test'?
radioisotope test, used to determine if the patient has a lack of IF
Why is the schillings test now rarely used clinically?
-can be difficult to interpret
What are the steps of the Schilling's test?
1) Oral radioactive B12 given
2) then i.m of non-radioactive B12 to saturate B12 binding
3) urine collected for 24hrs
normal person will excrete >10% in urine
From the Schilling's test, how much B12 will a normal person excrete in the urine?
Schilling's test: if it is
Repeat test with addition of oral IF
if now normal: pernicious anaemia or gastrectomy
if still abnormal: lesion in terminal ileum or bacterial overgrowth
Schilling's Test: Why is an i.m injection of non-radioisotope B12 part of the test?
To saturate binders, stopping their interference, so you get the 'true value' of B12 bound to IF and absorbed
What is autoimmune gastritis?
an inherited autoimmune disease that attacks parietal cells, resulting in decreased production of intrinsic factor. Consequences include atrophic gastritis, B12 malabsorption, and, frequently, pernicious anemia.
How would you look for evidence of autoimmune gastritis?
1) AB blood test (parietal cells and IF)
2) Biopsy with endoscopy
You've done an AB blood test to look for autoimmune gastritis, and you find AB against parietal cells. What does this mean?
Finding AB against parietal cells is helpful as it occurs in many people with AG,
BUT it is also present in some healthy people!
- = no pernicious anaemia
+ = inconclusive
You've done an AB blood test to look for autoimmune gastritis, and you find AB against intrinsic factor. What does this mean?
This is a very specific test, if you have these antibodies you DEFINITELY have pernicious anaemia
BUT some people with pernicious anaemia don't have this AB
What could you potentially see for a endoscopic biopsy for autoimmune gastritis?
- Evidence of AG
-Evidence of low acid output (raised plasma gastrin)
- Evidence of other autoimmune diseases (thyroid disease)
How long do our depleted B12 reserves take to 'run out'
Treatment of AG?
High replacement doses of B12 - 1000mcg every week for 4-6wks
then 1000mcg every 3 months
this is parenteral (intramuscular) due to impaired GI tract absorption, supplements wont work
Monitor response (B12 levels, haemoglobin/reticulocyte response, neurological symptoms)
What are the effects of terminal ileal resection
Loss of specialised receptors leading to
-failure to absorb B12
-failure to reabsorb bile salts, instead they are lost through the colon. This has an irritant effect of the colon > excessive fluid > diarrhoea
-impaired absorption of fats bc of reduced bile salts (high faecal fat)
Billroth 1 & 2 of distal gastrectomy
1) Antrum duodenum removed and rejoined 'end-to-end'
2) same antrum and duodenal removal, but duodenum end sown up, and instead jejunum is connected to the stomach
Why would you have low B12 after a partial gastrectomy?
No antrum > no G cells > low gastrin (reduced gastric acid secretion > hard to release B12 from food)(reduced pancreatic secretions)
No pylorus - bile can reflux back into stomach from duodenum (atrophic gastritis)
Body of stomach becomes inflamed and mucosa atrophies (degenerates)
-loss of parietal cells - loss of IF secretion
Some other causes of low B12 are?
Both B12 and folate are involved in? They are activated when
methylation pathway / DNA synthesis
Activated when B12 removes methyl group from flat
Sources of B12. therefore whos at risk? What are they made by?
meat and dairy
vegans and vegetarians at risk
made by bacteria
another name for vitamin B12
B12 Stored in ____ with the ____ for _____. How is it recycled
stored in the liver with R-binders for 2-3years. Recycled through bile.
Vitamin B12 absorption
1) vitB12/cobalamin is injested and needs to be seperated from the protein-food it comes in
2) this is done in the stomach by pepsin and HCl, Cbl released
3) R-proteins or hepatochorin (HC) from the saliva or stomach bind to the Cbl forming a HC.Cbl complex that travels to the duodenum
4) In the duodenum pancreatic proteases release Cbl from the HC.
5) Intrinsic factor present (from P cells) binds and forms a IF.Cbl complex that travels to the terminal ileum and is absorbed in the enterocytebrush border
6) travels to cells for DNA synthesis