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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 can cause Vitamin B12 deficiency?

A 
Dietary deficiency (vegans) 
Decreased absorption
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5
Q

What types of food have lots of folic acid?

A

Leafy green vegetables

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6
Q

Broadly speaking, what can cause folic acid deficiency?

A

Dietary deficiency
Increased demand for folate
Impaired absorption

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7
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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8
Q

What is folic acid required for?

A

DNA synthesis

Homocysteine metabolism

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9
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 by the action of B12 as a cofactor accompanied by the conversion of homocysteine to methionine.

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10
Q

In what reaction is B12 a co-factor?

A

The conversion of homocysteine to methionine

Enzyme = methionine synthetase

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11
Q

State some clinical features of B12 and folate deficiency.

A

(all rapidly dividing cells are affected)
Anaemia (macrocytic and megaloblastic)
Jaundice (due to ineffective erythropoiesis/breakdown of RBC’s)
Angular Cheilosis
Glossitis
Sterility
Weight loss and change of bowel habit

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12
Q

State some causes of macrocytic anaemia.

A
  1. Vitamin B12/Folate deficiency
  2. Liver disease and alcoholism
  3. Hypothyroidism
  4. Haematological disorders:
     Myelodysplasia (production of one or all types of blood cells by the bone marrow is disrupted)
     Aplastic anaemia (failure of blood cell production resulting in pancytopenia)
     Reticulocytosis (in response to haemolytic anaemia or bleeding)
  5. Drugs that interfere with DNA synthesis e.g azathioprine
  6. Prolonged nitrous oxide anaesthesia
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13
Q

How can you differentiate between the blood film of someone with B12/Folate deficiency and someone with liver disease or alcoholism causing macrocytosis?

A

B12/Folate deficiency = OVAL macrocytes

Liver disease and alcoholism = ROUND macrocytes

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14
Q

What is a reticulocyte?

A

A young red blood cell with no nucleus

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15
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
Basophilic (blue) to polychromatic to RBC (pink)

Their nucleus starts off being quite diffuse (open chromatin) and it becomes more and more compact until it is spit out by the red cell

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16
Q

Given your previous answer, 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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17
Q

What is meant by ‘megaloblastic changes’?

A

These are morphological 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.
You get an immature, open nucleus with mature cytoplasm.

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18
Q

Broadly speaking, what are megaloblastic changes the result of?

A

Defective DNA synthesis

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19
Q

Which of the causes of macrocytic anaemia also show megaloblastic changes in the bone marrow?

A

B12/Folate deficiency
Myelodysplasia
Drugs that interfere with DNA synthesis
Prolonged nitrous oxide anaesthesia

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20
Q

In megaloblastic anaemia, you see changes in the red blood cells and the white blood cells. Describe these changes.

A

Red blood cells
 Anisocytosis, Asynchrony between maturation of nucleus and cytoplasm (immature nucleus and mature cytoplasm)
 Large RBC’s, Increase in size of red cell precursors at all stages of maturation
 Increase in bone marrow activity because haemopoiesis is ineffective (dysplastic)
 Phagocytosis of dysplastic red blood cells
White blood cells
 Giant metamyelocytes (due to asynchronous maturation)
 Hypersegmented neutrophils

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21
Q

Which groups are at particular risk of dietary folate deficiency?

A

Elderly, sick, eating disorders, alcoholics

22
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)

23
Q

State some physiological and pathological causes of increased folate demand.

A 
Physiological (increased growth) 
 Pregnancy
 Adolescence 
 Premature babies
Pathological (rapid cell turnover) 
 Malignancy 
 Erythroderma (whole body rash)
 Haemolytic anaemia
24
Q

State some causes of malabsorption of folate.

A

Coeliac Disease
Surgery or inflammatory bowel disease (e.g. Crohn’s disease)
Drugs (e.g. colestyramine, sulfasalazine and methotrexate)

25
Q

What is coeliac disease caused by?

A

Sensitivity to gliadin (group of proteins found in wheat) leads to subtotal villous atrophy with crypt hyperplasia in the duodenum.

26
Q

How can coeliac disease be diagnosed?

A

Anti-gliadin (transglutaminase) antibodies

Duodenal biopsy

27
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

28
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

29
Q

What are the three main consequences of folate deficiency?

A
  1. Megaloblastic anaemia
  2. Neural tube defects in developing foetuses
  3. Increased risk of venous thromboembolism
30
Q

What are the two types of neural tube defects?

A

Spinal cord = spina bifida

Brain = anencephaly

31
Q

What are the NICE guidelines for women of standard and high risk of neural tube defects?

A

Standard Risk – 400 mcg folic acid preconception to 12 weeks gestation
High Risk – 5 mg folic acid preconception to 12 weeks gestation
Haemolytic anaemia – 5-10 mg before, during and after pregnancy

32
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 and probably with arterial and venous thrombosis.

33
Q

How did the FDA in the USA attempt to reduce the incidence of NTDs due to folate deficiency?

A

Fortify grain with folate

34
Q

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

A

Vegans

35
Q

State some factors that can affect the absorption of B12.

A
  1. Reduction in intrinsic factor
    - post gastrectomy
    - gastric atrophy
    - autoimmune – pernicious anaemia
    a. either presence of IF-antibodies
    b. parietal cell antibodies, 90% in adults with PA but 16% of normal women over 60
  2. Diseases of the small bowel (and terminal ileum)– Crohn’s, Coeliac, surgical resection
  3. Infections
    - H.pylori
    - giardia
    - fish tapeworm
    - bacterial overgrowth
  4. Drugs associated w/low B12
    - metformin
    - proton pump inhibitors e.g omeprazole
    - oral contraceptive pill
36
Q

What are the neurological consequences of B12 deficiency?

A

Neurological problems due to demyelination

  • Subacute combined degeneration of the spinal cord leads to paralysis
  • bilateral peripheral neuropathy
  • optic atrophy
  • dementia
37
Q

What is the relationship between Hb level and neurological symptoms in B12 deficiency?

A

Inverse relationship between Hb level and neurological symptoms

38
Q

What is subacute combined degeneration of the spinal cord and what are the symptoms?

A

Caused by demyelination of the posterior (dorsal) and lateral (pyramidal) tracts of the cervical and thoracic spinal cord
Results in loss of joint position sense and vibration sense.
Patient may have a wide-based gait and sometimes experience pain.

39
Q

State some symptoms and signs of B12 deficiency.

A
  1. ROMBERG’S SIGN, loss of proprioception
  2. Paraesthesia (tingling, prickling sensation)
  3. Muscle weakness
  4. Difficulty walking
  5. Anaemia and jaundice giving ‘yellow tinge’
  6. Visual impairment
  7. Psychiatric disturbance
  8. Absent reflex, up-going plantar reflex
40
Q

What can you measure in patients w/low B12?

A
  1. Antibodies to parietal cells and IF
  2. Antibodies for coeliac disease
  3. Breath test for bacterial overgrowth
  4. Stool test for H.pylori and a test for Giardia
  5. Schilling test
41
Q

What is the role of B12 in DNA synthesis?

A

Both B12 and folate are needed for the production of dTMP (deoxythymidine), which is a crucial building block in DNA synthesis

42
Q

State some new tests used to diagnose B12 deficiency.

A 
Plasma homocysteine (high in B12 and folate deficiency) 
Serum methyl malonic acid levels  
Holotranscobalamin levels (transcobalamin II)
43
Q

What is the Schilling test for B12 absorption?

A

Part 1
-give injections of B12 to replenish stores and patient drinks radio labelled B12
would normally expect to see B12 in urine as stores are full
if none in urine, two possibilities:
1. not absorbing B12, pernicious anaemia, small bowel disease
2. hasn’t corrected B12 deficiency before test
Part 2
-repeat test with addition of IF and measure excretion of B12 in the urine

44
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

45
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)

46
Q

How is B12 deficiency treated?

A

Injections of B12 (1000mcg), 3x a week for 2 weeks thereafter every 3 months
If neurological involvement, B12 injections alternate days until no further improvement (3 weeks) thereafter every 2 months

47
Q

What three things are essential for B12 absorption?

A
  1. Intact stomach
  2. Intrinsic factor
  3. Functioning small intestine
48
Q

What does a low result in Part 1 and a normal result in Part 2 in the Shilling test indicate?

A

P1 LOW
P2 NORMAL
Pernicious anaemia with auto antibodies to the B12

49
Q

What does a low result in Part 1 and a low result in Part 2 in the Shilling test indicate?

A

Malabsorption due to coeliac, bacterial overgrowth

50
Q

What are the two methods of absorption of B12?

A

Occurs in small intestine
Method 1- (1%)
Slow and inefficient happens in DUODENUM

Method 2- (99%)
B12 must combine with intrinsic factor
Intrinsic factor is made in the stomach 
(parietal cells)
B12-IF binds to ileal receptors
51
Q

What is the most common cause of B12 deficiency?

A

Poor absorption

Haematology (11 decks)

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