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MDCN 350: Course 1 > Anemia and the Micronutrients: B12, Folate and Iron > Flashcards

Anemia and the Micronutrients: B12, Folate and Iron Flashcards

1
Q

Reasons behind increased MCV

A 
B12 deficiency
folate deficiency
Drugs
reticulocytosis
liver disease
hypothyroidism
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2
Q

reasons behind normal MCV

A 
bleeding
hemolysis
marrow failure
renal disease
endocrine disease
anemia of chronic disease
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3
Q

reasons behind decreased MCV

A

Fe2+ deficinecy
Thalassemia
Lead poisoning
Anemia of chronic disease.

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4
Q

what part of GI tract is folate absorbed? B12?

A

folate: jejunum
B12, Mg2+, Ca2+ and cobalamine: ileum.

everything else ex/ fat soluble vitamins, iron, zinc, water soluble vitamins etc get absorbed in duodenum and jejunum.

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5
Q

where is most of the body’s iron

A

presnt in Hb in circulating red cells, some in macrophages

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6
Q

the macrophages of the reticuloendothelial system store iron released from Hb as ___ and ___

A

ferritin and homosiderin

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7
Q

daily internal requirements of iron for production of Hb are _____ per day

A

20-25mg/day from recycling from red cell destruction and from releases from tansferring (food)

liver iron stores 1g (less in menstruating women and growing children)

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8
Q

where can you find metabolically active iron

A
  1. Hb (2g)
  2. seron iron bound to a protein TRANSFERRIN in blood (3mg)
  3. Tissue iron: in cytochromes and enzymes (8mg)
  4. Myoglobin (oxygen reserve in muscles (130mg)
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9
Q

what is storage iron

A

ferritin: found in blood, tissue fluids and cells. When tested, it tells us a good total store of Fe stores in the body

Haemosiderin: found in macrophages and assessed by staining bone marrow.

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10
Q

inorganic vs organic iron sources from diet

A

inorganic: non-heme iron like lentils. harder to absrob iron from.
organic: beef

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11
Q

where is iron mainly absorbed in the body

A

in the duodenum, whereas b12 is in the ileum and folate in the jejunum.

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12
Q

the quantity of iron absorbed is regulated by ___

A

enterocytes. Haem iron enters the enterocyte through different processes than inorganic non heme iron.

from the lumen, Fe3+ gets converted to Fe2 + and absrobed into the enterocyte. Fe2+ can either be stored as ferritin or can make it’s way into the blood stream where it binds with transferritin for transport.

Only Fe2+ can be absorbed!

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13
Q

daily iron requirement

A

10-15mg/day (5-10% absorbed)

  • a western diet typically contains about 15 mg of iron. 30% of dietary iron is promptly absorbed via its own transport mechanis,
  • a heme iron transport HEME CARRIER PROTEIN 1 (HCP1) has been found in the apical brush border of the duodenal enterocyte.
  • the remaining iron is poorly absorbed with less than 10% being taken into mucosal cells.
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14
Q

Typically, at physiological pH, ferrous dietary iron (Fe2+) is rapidly oxidized to the insoluble ferric (Fe3+) form. How does it get converted back to fe2+ so enterocytes can absorb them into Gi cells?

A

gastric acid lowers the pH in the proximal duodenum, converting ferric to ferrous enhancing uptake. Fe3+ to Fe2+ can also be done by a reductase on the brush border.

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15
Q

T/F: Heme carrier protein 1 on the apical brush border of the duodenal enterocyte also transports Fe2+

A

false. it only transports heme iron. Fe2+ is absorbed in the enterocytes/transported into the cell through divalent metal transferase1 (DMT1) receptor.

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16
Q

competitors or iron absorption

A

lead, cobalt, strontium, manganese, zinc.

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17
Q

facilitators of iron absorption

A

ascorbate, citrate, amino acids, iron deficiency.

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18
Q

inhibitors of iron absorption

A

plant phytates, soil, clay, antacids. tes coffee/phenolic compounds.

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19
Q

Fe2+ enters the enterocyte from the lumen via ___ transporter. from there it can be stored as __ or used. the Fe2+ in the enterocyte can be transported into the blood tream via ___ and ___ (needs Cu2+ for activation), where it can go around th ebody and into macrophages for storage as ferriten or where it can be bound to _____ on erythroid progenitors for Hb production.

A

Fe2+ enters the enterocyte from the lumen via DMT1 transporter. from there it can be stored as __ or used. the Fe2+ in the enterocyte can be transported into the blood tream via FERROPORTIN and HEPHAESTIN (needs Cu2+ for activation), where it can go around th ebody and into macrophages for storage as ferriten or where it can be bound to TRANSFERRING on erythroid progenitors for Hb production.

see slide 20 on lecture notes.

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20
Q

why can too much hepcidin affect the iron stores or Hb production in your body

A

beacuse it can inhibit ferroportin, which is the transporter that facilitates the movmenet of Fe2+ from the enterocytes to the blood stream. It can also cause any Fe2+ to be cloistered in the macrophages rather than being released to erythroid progenitors for Hb production.

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21
Q

iron deficiency anemia is characterized by a ___ MCV

A

decreased. microcytic anemia.

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22
Q

etiologies behind iron deficiency anemia

A
  1. decreased iron intake
  2. decreaed iron absorption (celiac, Chrohns (B12) deficiency)
  3. increased iron LOSS: Chronic bleeding
    - menorrhagia/ pregnancy
    - peptic ulcer
    - stomach ulcer
    - inflammatory bowel disease (UC)
    - intestinal cancer
    - haemorrhoids (uncommon)
    - Blood donation
  4. increased iron requirements (pregnancy, lactation.
    - any surgery that results in removal of partial duodenum like gastric bypass will put someone at risk for iron deficiency
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23
Q

major causes of microcytic anemia

A
  • Fe deficiencies based on flaws of intake/absorption/loss/dif iron requirements etc.
  • thalassemia
  • lead poisoning
  • inflammation anemia
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24
Q

small RBC always indicates a ___ maturation defect associated with a decrease in __ synthesis

A

indiactes a cytoplasmic maturation defect associated with a decrease in Hb synthesis.
cuases include: Fe deficinecy, thalassemia, lead poisoning, anemia of inflammation

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25
Q

clinical presentation of Fe deficinecy

A
  • PALLOR in the conjunctiva
  • clubbing of nails Koilonychia
  • fatigue and irritability
  • angular stomatitis (sore on corner of lips)
  • blue sclera
  • pica
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26
Q

lab tests/investigations that may indicate microcytic/Fe deficient anemia

Ferritin: 
- Serum iron: 
total iron binding capacity (TIBC): 
- transferrin Saturation: 
- Soluble transferring receptor:
A
  • Ferritin: usually low in Fe deficiency
  • Serum iron: low
    total iron binding capacity (TIBC): HIGH
  • transferrin Saturation: LOW
  • Soluble transferring receptor: elevated
  • Gold standard is bone marrow biopsy (RARE)
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27
Q

Treatment of microcytic anemia because of Fe Deficiency (remember microcytic anemia coud also be due to thalassemia, anemia of chronic disease, or Pb poisoning)

A

Oral ion– start slow as very constipating and may cause nausea and stomach cramps

IM iron: painful, but can give large doses

IV iron: needs to be done in hospital and takes many hours and may cause serum sickness, fever, headaches

28
Q

treatment for lead poisoning that is causing microcytic anemia. And key histological finding of Pb poisoning

A

chelation. you often see basophilic stippling

Pb poisoning is interesting because in addition to microcytic anemia/irritability/ etc it also causes cognitive impairment.

29
Q

treatment for lead poisoning that is causing microcytic anemia. And key histological finding of Pb poisoning

A

chelation. you often see basophilic stippling

Pb poisoning is interesting because in addition to microcytic anemia/irritability/ etc it also causes cognitive impairment.

30
Q

the first step when assessing anemia with elevated MCV (macrocytic anemia) is to:

A

rule out reticulocytosis

See black book slides for “anemia with elevated MCV” – or slide 35

31
Q

in patients with macrocytosis there is a ___ ___ defect in bone marrow ____ ____ cells associated with decreased Hgb synthesis.

A

in patients with macrocytosis there is a NUCLEAR MATURATION defect in bone marrow RBC PRECURSOR cells associated with decreased Hgb synthesis.

32
Q

macrocytes from B12 or folate deficiency are the result of:

A

skipped mitoses, so their volume is about twice that of other RBC.

33
Q

causes of increased MCV

A

B12 or folate deficiency, drugs like vasothiaprin, abnormal RBC maturation, or liver disease, hypothyroidism, alcohol abuse, and reticulocytosis.

34
Q

macrocyte shape

A

macroovalocytes. oval looking cells.

35
Q

ddX of macrocytic anemia

A
  • B12 deficiency
  • Folate deficiency
  • myelodysplasia
  • reticulocytosis
  • hypothyroidism
  • liver disease if theres random macrocytes
  • certain drugs like hydrea or AZT
36
Q

Folic acid vs folate

A

folic acid is the oxidized form of the vitamin found in fortified foods and supplements
- folate is the reduced form found naturally in foods and tissues.

37
Q

3 components of folate

A
  • pterdine
  • PABA
  • Glutamic acid
38
Q

how much folate should you ingest a day to prevent folate deficiency

A
  • 100-400 ug/day
39
Q

best marker of folate deficiency

A

RBC folate– serum albumin can give falsely low folate levels because 60-70% of serum folate is bound to proteins.

40
Q

why is it super easy to become folate deficient?

A

folate is H2O soluble with increased turnover. Its easy to get deficient because theres minimal storage.

41
Q

4 functions of folate

A
  1. DNA synthesis:
  2. important role in formation of the neural tube during development
  3. protein synthesis
  4. involved in the metabolsim of homocysteine: folate works with B12 to make methionine out of homocysteine.
42
Q

What can happen if you’re deficient in B12 and folate?

A

can cause hyperhomocysteinemia because both are involved in turning homocysteine into methionine (thus involved in protein synthesis– methylated homocyteine). Without folate and B12, there will be an accumulation of homocysteine.

hyperhomocyteinemia is associated with increased risk for coronary artery disease, venous thromboembolus, and stroke.

43
Q

How can you use biochemical values to assess B12 or folate values?

A

both are involved in methionine synthesis out of homocysteine. if you have a build up of homocysteine, you know you’re deficient in either B12 or folate.

To know if theres a B12 problem, you should also look at methylmalonyl coA. if theres a lot of methylmalonyl coA, then theres a deficiency in B12 because B12 is involved in converting it to succinyl coA.

If there’s increased methylmalonyl coA and homocysteine, you can tell you’re deficiency in both B12 and folate.

If there’s no increased methylmalonyl coA but theres an increase in homocysteine, then you have adequate levels of B12 but not enough folate.

44
Q

for folate digestion, absorption, etc. Polyglutamate forms of folate must be hydrolyzed to monoglutamate forms. Two intestinal protiens are required for the sequential hydrolysis of dietary poyglutamates and transport of derivatives across the enterocyte brush border are:

A
  1. glutamate carboxypeptidase II

2. reduced folate carrier RFC

45
Q

after folate is transported into the cell, folate is ___ and ___ to the form Tetrahydrofolate (THF)

A

reduced and methylated. THF is then transported across the intestinal basolateral membrane by RFC to the portal vien and liver.

46
Q

how does a basic PH environment influence folate?

A

it decreases absorption.

47
Q

drugs that decrease folate absorption

A

-methotrexate, sulfasalazine (inflammatory), phenytoin, carbamazpine, alcohol.

48
Q

which WBC could indicate a B12 deficiency?

A

neutrophils with more than 3 lobes/ hypersegmented neutrophil

49
Q

what is megaloblastic anemia

A
  • fewer RBC made
  • RBC larger than normal
  • RBC do not carry oxygen as effectively because theres less of them.
  • often with elevated homocysteine levels.
  • due to B12 or folate deficiency
50
Q

how do you diagnose a folate deficiency? Treatment for folate deficiency?

A
  • serum folate –> not re`ally good cause it fluctuates a lot
  • red blood cell folate –> more accurate, check B12 at the same time.
  • treatment with oral supplementation, or less commonly, parenteral therapy
51
Q

how do you diagnose a folate deficiency? Treatment for folate deficiency?

A
  • serum folate –> not re`ally good cause it fluctuates a lot
  • red blood cell folate –> more accurate, check B12 at the same time.
  • treatment with oral supplementation, or less commonly, parenteral therapy
52
Q

absorption of B12 requires 5 factors

A
  1. adequate dietary intake
  2. acid-pepsin in the stomach
  3. IF
  4. pancreatic proteases
  5. intact ileum with B12-IF receptors
53
Q

causes of B12 deficiency

A
  1. poor intake
  2. Cbl not freed in the stomach antrum
  3. lack of IF
  4. Pancreatic insufficiencies
  5. bacterial consumption
  6. ileum mucosal abnormality
  7. lack of TACII
54
Q

Schilling Test

A

procedure done to look at the B12 absorption

  1. give radioactive Cbl orally and then IM unlabelled CBl. Look at urine 24 hours later
  2. Give Cbl with IF and see if abnormal urine B12 amounts resolve
  3. Give Cbl with antibiotics and see if abnormal urine B12 amounts resolve.
55
Q

outline the mechanism of B12 absorption

A
  1. Dietary B12 /Cbl consumed
  2. released from good with low pH (ie in stomach H+ from parietal cells)
  3. Binds to R protein (from salivary glands)
  4. pancreatic enzymes cleave R-Cbl allowing Cbl to bind to IF (secreated by parietal cells)
  5. IF-Cbl absorbed by binding to the IF-receptor in the terminal ileum
  6. IF-Cbl complex is internalized and in the enterocyte Cbl is transferred to transcobalamin II (TCII)
  7. TCBII-Cbl is transported out the enterocyte and into the circulation
56
Q

B12 deficiency- etiologies:
- dietary deficiency is usually very rare in food of animal origin. B12 deficiency is usually due to malabsorption; with the commonst cuase due to:

A

lack of intrinsic factor (recall that IF binds to Cbl so that it can bind to receptors on the terminal ileum and facilitate Cbl to be internalized in the enterocyte.

  • IF lack might be due to an autoimmune disorder, a gastrectomy, or diseases of small bowel.
57
Q

Feature of B12 deficiency

A
  • macrocytic-megaloblastic anemia
  • hypersegmented neutrophils (more than 3 lobes)
  • fatigue, weighloss, diarrhea, loss of appetite, fever, sore, tongue, hair loss.
  • paraesthesia, dementia, neuropathy, demyelination of spinal cord.

*not being anemic does not exclude B12 deficiency. Can still have neurlogical problems. Folate doesn’t cause neuro problems.

NOTE: neuropsychiatric symptoms are often seen in the absense of anemia, macrocytosis or both. Anemia is often seen without neurologic symptoms. MCV does not predict degree of deficiency.

58
Q

diagnostic tests to determine B12 deficiency

A

the CBC
B12 level

Homocystein and mathylmalonic acid test (recall: if you have a lot of methylmalonic acid that isn’t being converted to succinyl coA, there could be a B12 deficiency).
- can look at antibodies to parietal cell and IF to see if there’s an IF problem.

59
Q

peripheral blood findings in B12 deficiency

A
  • anemia with ovalomacrocytes
  • low WBC
  • low platelets
  • hypersegmented neutrophils
60
Q

peripheral blood findings in B12 deficiency

A
  • anemia with ovalomacrocytes
  • low WBC
  • low platelets
  • hypersegmented neutrophils
  • MCV often elevated, but may be normal if very severe, precipitous, or concurrent Fe deficiency.
61
Q

Diagnosing Vitamin B12 deficiency

A
  • low serum vit B12 levels
  • confirm if borderline test with methylmalonic acid +/- homocysteine
  • demonstrate B12 malabsorption via Schilling test: malabsorption of vitamin B12 corrected by IF= IF deficiency
62
Q

confounds as to why there might be a HIGH B12

A

recent multivitamin ingestion is a major factor.

63
Q

pernicious anemia

A

deficiency in RBCs caused by lack of vitamine B12 in the blood. PA is defined as a type of vittamine B12 deficiency that results from impaired uptake of vitamin B12 due to the lack of a substance known as IF

64
Q

which types of antibodies are often seen in someone with pernicious anemia?

A

antiPARIETAL CELL antibodies. H+ secreted by these cells usually are able to release Cbl from food. antiparietal cell abs are seen in 85% of patients with pernicious anemia.
- also thought to have a causative role in chronic atrophic gastritis and pernicious anemia.

  • rarely prsent in health people or in patients without autoimmune disorders, so it’s highly sepcific (even though the test is kind of insensitive)
65
Q

can patients with pernicious anemia be treated with oral B12?

A

YES BUT LIMITED:

PA is when IF antibodies are produced, so that the cells that make IF are compromised. Results in decreased IF in the terminal ileum and thus reduced B12 absorption. thus more B12 won’t help. You need things to mitigate IF degradation which is hard.

Give oral B12 ( a lot of it) so that some can passively go through without relying on IF.

raditionally, vitamin B12 replacement is administered intramuscularly. However, it is believed that oral vitamin B12 can be absorbed passively independent of intrinsic factors. Passive diffusion accounts for about 1% of total absorption, and this route of absorption is unaffected in patients with pernicious anemia

66
Q

oral dose of B12

A

300-1000 ug/Day

  • typical multivitamines have <10 ug/B12
  • efficacy has been demonstrated in a randomized study of IM versus PO B12
67
Q

treatment of vitamin B12 deficiency

A
  • parenteral vit B12 injections
  • frequeny injections
  • maintenance injections monthly for life if pernicious anemia (since IF will always be negatively affected)
  • Oral Vitamin B12 supplements (high dose)

MDCN 350: Course 1 (48 decks)

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