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Haematology > Vitamin B12 And Folic Acid Deficiency > Flashcards

Vitamin B12 And Folic Acid Deficiency Flashcards

1
Q

What is vitamin B12 and what types of food is it commonly found in?

A

Cobalamin (vitamin B12) is a bacterial product that is ingested and stored by animals.
It is found in meat, cheese, salmon, cod, milk, eggs

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2
Q

How much B12 is needed every day and how much is found in hepatic stores?

A

1.5-3 mcg/day required

Store: 2-5 mg (will last several years)

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3
Q

What is Vitamin B12 needed for?

A

DNA synthesis

Integrity of the nervous system (involved in myelination)

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4
Q

Broadly speaking, what tends to cause Vitamin B12 deficiency?

A 
Dietary deficiency (vegans) 
Decreased absorption
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5
Q

What is folic acid required for?

A

DNA synthesis

Homocysteine metabolism

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6
Q

What is the dietary requirement of folic acid?

A

400-600 mcg

You run out of folate much quicker than B12

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7
Q

Broadly speaking, what can cause folic acid deficiency?

A
  • Dietary deficiency
  • Increased demand for folate
  • Impaired absorption
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8
Q

Deoxythymidine (dTMP) is a major building block of DNA synthesis. How is it produced?

A

It is produced by the methylation of deoxyuridine (dUMP)
For the methylation to take place, you need the release of methyl groups from methyl-tetrahydrofolate (derived from dietary folate) by the action of B12 as a cofactor accompanied by the conversion of homocysteine to methionine.

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9
Q

In what reaction is B12 a co-factor? State the enzyme.

A

The conversion of homocysteine to methionine

Enzyme = methionine synthetase

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10
Q

State some clinical features of B12 and folate deficiency.

A
  • Anaemia (macrocytic and megaloblastic)
  • Jaundice (due to ineffective erythropoiesis)
  • Angular Cheilosis
  • Glossitis
  • Sterility
  • Weight loss and change of bowel habit
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11
Q

State some causes of macrocytic anaemia.

A
  • Vitamin B12/Folate deficiency
  • Liver disease and alcoholism
  • Hypothyroidism
  • Drugs that interfere with DNA synthesis e.g. azathioprine

Haematological disorders:

  • Myelodysplasia
  • Aplastic anaemia (failure of blood cell production resulting in pancytopenia)
  • Reticulocytosis (in response to haemolytic anaemia or bleeding)
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12
Q

Describe how the appearances of cells of the red cell lineage change as they mature.

A

They become smaller and their cytoplasm becomes pinker
Their nucleus starts off being quite diffuse (open chromatin) and it becomes more and more compact/pyknotic until it is spit out by the red cell => reticulocyte (young red blood cell with no nucleus)

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13
Q

Hence, what two things do you look at when determining the maturity of a red blood cell?

A

Chromatin – how open is it?

Colour of the cytoplasm – how blue is it?

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14
Q

What is meant by ‘megaloblastic changes’?

A

These are changes seen in the red blood cell precursors in the bone marrow.
Megaloblastic change is when there is asynchronous maturation of the nucleus and cytoplasm => immature, open nucleus with mature cytoplasm

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15
Q

What changes are seen in the peripheral blood in megaloblastic anaemia?

A
  • Anisocytosis
  • Large red cells
  • Hypersegmented neutrophils
  • Giant metamyelocytes (due to asynchronous maturation)
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16
Q

Give 3 tests that you would do if someone had a macrocytosis

A

B12/folate measurement
thyroid function test
liver function test
Reticulocyte count

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17
Q

Which groups are at particular risk of dietary folate deficiency?

A

Elderly, sick, eating disorders, alcoholics

18
Q

What are the consequences of folate deficiency for DNA synthesis?

A

Folate deficiency means that you can’t methylate dUMP to dTMP, which affects DNA synthesis.
It also leads to the accumulation of homocysteine (it can’t be converted to methionine without folate)

19
Q

What food is high in dietary folate? What is it destroyed by?

A

Fresh leafy vegetables

Destroyed by overcooking/canning/processing

20
Q

State some physiological and pathological causes of increased folate demand (which if unaccounted for would cause a folate deficiency).

A

Physiological (times of increased growth)

  • Pregnancy
  • Adolescence
  • Premature babies

Pathological (rapid cell turnover)

  • Malignancy
  • Erythroderma (whole body redness and eczema)
  • Haemolytic anaemia
21
Q

State some tests to identify folate deficiency.

A
  • Full blood count
  • Blood film
  • Serum folate (useful as a screening test);
    Shows diurnal variation
    Affected by recent changes in diet
  • Red cell folate – useful as confirmatory test
22
Q

What would you expect the serum folate and red cell folate of a patient with B12 deficiency to be and why?

A

Serum folate = high
Red cell folate = LOW
This is because B12 is required for the folate to enter the red blood cells

23
Q

What are the three main consequences of folate deficiency?

A
  • Megaloblastic anaemia
  • Neural tube defects (e.g. spina bifida, anencephaly)
  • Increased risk of venous thromboembolism in association with variant enzymes involved in homocysteine metabolism
24
Q

How much folic acid should all pregnant women take?

A

0.4mg/day prior to conception and for the first 12 weeks

25
Q

Homocysteine accumulates in folate deficiency. What are the consequences of this?

A

Very high homocysteine levels are associated independently with:

  • atherosclerosis
  • premature vascular disease

Mildly elevated homocysteine is associated with

  • cardiovascular disease (definitely)
  • arterial and venous thrombosis (probably)
26
Q

How did the FDA in the USA attempt to reduce levels of folate deficiency?

A

Grains fortified with folic acid

27
Q

Which groups of people are at particular risk of vitamin B12 deficiency due to decreased dietary intake?

A

Vegans

28
Q

Describe briefly how B12 is absorbed, hence stating the 3 essential things to ensure proper absorption

A

Method 1 of absorption (1%):

  • duodenum
  • slow and inefficient

Method 2 of absorption (rest):

  • B12 must combine with intrinsic factor
  • Intrinsic factor is made in the stomach (by parietal cells)
  • B12-IF binds to ileal receptors

Hence, 3 things are essential:

  1. Intact Stomach
  2. Intrinsic factor
  3. Functioning small intestine
29
Q

Say how impaired B12 absorption due to reduction in intrinsic factor may arise

A
  • Post-gastrectomy
  • Gastric atrophy
  • Antibodies against intrinsic factor or parietal cells = pernicious anaemia
30
Q

Say how impaired B12 absorption due to diseases of small bowel (terminal ileum) may arise

A
  • Crohns
  • Coeliac disease
  • Surgical resection
  • Infections e.g. H. Pylori, Giardia, Fish tapeworm, Bacterial overgrowth
31
Q

State 3 drugs that are associated with low B12

A
  1. Metformin
  2. Proton pump inhibitors e.g. omeprazole (used to treat GER)
  3. Oral contraceptive pill
32
Q

What are some of the neurological problems associated with B12 deficiency?

A
  • Bilateral peripheral neuropathy
  • Subacute combined degeneration of the cord
  • Optic atrophy
  • Dementia
33
Q

Give some symptoms that the patient with B12 deficiency may experience

A
  • Paraesthesiae
  • Muscle weakness
  • Difficult walking
  • Visual impairment
  • Psychiatric disturbance
34
Q

What might you note about someone with B12 deficiency upon a neuro examination?

A
  • Absent reflexes and upgoing plantar responses

- Loss of proprioception so falls over when they close their eyes (= Romberg’s sign)

35
Q

What is subacute combined degeneration of the spinal cord?

A

Caused by demyelination of the posterior (dorsal) and lateral (pyramidal) tracts of the cervical and thoracic spinal cord

36
Q

What is pernicious anaemia and what does it result in?

A

A form of anaemia resulting from the deficiency of B12
It can be caused by autoimmune atrophic gastritic with the loss of intrinsic factor
This results in macrocytic/megaloblastic anaemia with or without neurological damage

37
Q

Which antibodies are found in pernicious anaemia?

A
  • Anti-intrinsic factor antibodies (in 40-60% of adults with PA)
  • Anti-gastric parietal cell antibodies (in 80-90% of adults with PA)
38
Q

Describe the Schilling test for B12 absorption?

A

Prior to test, replenish B12 stores:

a) drink radiolabelled B12
b) measure excretion in the urine

Then repeat test with the addition of intrinsic factor.

39
Q

What are some other tests used to diagnose B12 deficiency.

A
  • Plasma homocysteine

- Serum methyl malonic acid levels

40
Q

How are folate and B12 deficiency treated?

A
  • Oral folate or oral cyanobalamin (manufactured form of B12) for dietary deficiency or increased demand
  • Intra muscular injections of B12 (1000micrograms) for malabsorption due to pernicious anaemia or bowel disease

Haematology (11 decks)

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