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Haematology > Vitamin B12 and Folic Acid Deficiency > Flashcards

Vitamin B12 and Folic Acid Deficiency Flashcards

1
Q

What are the haematinics?

A

iron, B12 and folate - vitamins needed to make blood

Deficiencies cause anaemia

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2
Q

What are vitamin B12 and folate needed for?

A

DNA synthesis

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3
Q

What else does vitamin B12 do?

A

It affects the CNS and PNS

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4
Q

What is the other role of folic acid?

A

Needed in homocysteine metabolism

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5
Q

Which molecule in DNA are folic acid and B12 needed to make?

A

deoxythymidine (it is made from deoxyuridine by adding a methyl group). The methylation needs folic acid to be changed into different forms and B12 as a cofactor

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6
Q

Which parts of the body will be affected by B12 and folate deficiency? Where will the effects be worst?

A
  • All rapidly dividing cells will be affected, because you cannot make DNA properly
  • Effects are worse in bone marrow, epithelial surfaces of the mouth/gut, the gonads and in embryogenesi
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7
Q

What are the clinical features of B12 and folate deficiency?

A
  1. Anaemia – this can lead to weakness, tiredness and
  2. This type of anaemia involves the breakdown of lots of cells -> jaundice
  3. GI tract affected so glossitis (inflamed tongue) and angular cheilosis (inflamed corners of mouth)
  4. Weight loss
  5. Change in bowel habit
  6. Sterile (sperm not properly made)
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8
Q

What type of anaemia occurs in B12 and folate deficiency?

A

Macrocytic: large RBC, high MCV

Megaloblastic: Morphological change in RBC precursors in bone marrow

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9
Q

What can cause macrocytic anaemia?

A
  • Vitamin B12/folate deficiency
  • Liver disease or alcohol
  • Hypothyroidism (thyroid disease can cause macrocytosis but NOT megaloblastic change)
  • Drugs e.g. azathioprine (immunosuppressant)
  • Haematological disorders: myelodysplasia, aplastic anaemia, reticulocytosis (chronic haemolytic anaemia)
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10
Q

What are the stages in a RBC differentiation?

A

Erythroblast -> normoblast -> reticulocyte -> RBC

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11
Q

What happens to the red cell nucleus and cytoplasm through the stages of differentiation?

A

Nucleus gets smaller and smaller until it becomes pyknotic

The cytoplasm gets pinker as the amount of Hb increases

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12
Q

What is pyknosis?

A

Pyknosis is the irreversible condensation of chromatin in the nucleus of a cell. It is followed by karyorrhexis (fragmentation of the nucleus).

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13
Q

What is megaloblastic anaemia?

A
  • DNA is not being produced in the normal way

- It is defined by asynchronous maturation of the nucleus and cytoplasm in the erythroid series

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14
Q

What would stained RBCs in megaloblastic anaemia look like?

A

You may see cells with blue cytoplasm and no nucleus, or pink cells with a nucleus

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15
Q

Describe what may be seen in a peripheral blood smear in megaloblastic anaemia?

A
  • large red cells
  • hypersegmented neutrophils
  • giant metameylocytes (immature neutrophils)
  • anisocytosis (uneven RBC size)
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16
Q

Where is the main megaloblastic change?

A

In the bone marrow

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17
Q

What does megaloblastic change tell us?

A

There is B12 or folate deficiency

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18
Q

Where do we get folate from?

A

Folate is found in fresh or frozen leafy vegetables

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19
Q

Why may folate deficiency occur?

A
  • It can be destroyed by overcooking/canning/processing
  • Folate deficiency can be caused by decreased intake: ignorance, poverty
  • Folate deficiency is often seen in the elderly and in alcoholics
  • Increase demand
20
Q

What are the physiological and pathological reasons behind increased folate deficiency?

A

Physiological: pregnancy, adolescence, premature babies

Pathological: malignancy, erythroderma, haemolytic anaemias

21
Q

What tests are done to diagnose folate deficiency?

A
  • Do a full blood count and blood film

- Serum folate levels in the blood

22
Q

How is the cause of low folate assessed?

A
  • Take a history (diet/alcohol/illness)

- Examination (skin disease/alcoholic liver disease)

23
Q

What are the consequences of folate deficiency?

A
  1. Megaloblastic, macrocytic anaemia
  2. Neural tube defects in developing foetus
  3. Increased risk of thrombosis in association with variant enzymes involved in homocysteine metabolism
24
Q

Which neural tube defects could occur due to folate deficiency and how is this avoided?

A

Spina bifida and anencephaly (absence of majority of brain, skull and scalp)

All pregnant women take folic acid 0.4mg prior to conception, and for the first 12 weeks of pregnancy.

25
Q

Homocysteine, methionine and their toxicities

What are high homocysteine levels associated with?

A
  • There’s a step in the folate pathway that involves B12, in which homocysteine is converted to methionine
  • Homocysteine and methionine are both essential amino acids, but homocysteine is toxic
  • Very high homocysteine levels are associated with atherosclerosis and premature vascular disease
26
Q

What are mildly high levels of homocysteine associated with?

A
  • Cardiovascular disease (definitely)
  • Arterial thrombosis (probably)
  • Venous thrombosis (possibly
27
Q

What are the consequences of B12 deficiency (neurological)?

A
  • Bilateral peripheral neuropathy
  • Subacuate combined degeneration of the cord (posterior and pyramidal tracts of the spinal cord)
  • Optic atrophy
  • Dementia
28
Q

What are the symptoms of B12 deficiency?

A
  • Paraesthesiae (sensation)
  • Muscle weakness
  • Difficult walking
  • Visual impairment
  • Psychiatric disturbance
  • Upper and lower motor neurone signs e.g. Babinksi’s
  • Loss of propriception (Romberg’s sign)
29
Q

What are the causes of B12 deficiency?

A

People shouldn’t become deficient just because they are growing fast.

  • poor absorption
  • reduced dietary intake (stores last 4 years)
  • infections/infestations (they consume it e.g. tropical sprue, abnormal bacterial flora, fish tapeworm)
30
Q

Do we have large or small stores of folate/B12?

A

folate - small

B12 - large

31
Q

Where is B12 found and how is at risk of developing it?

A
  • In all animal produce (e.g. in meat, fish and dairy products)
  • Vegans are at risk of B12 deficiency
32
Q

What is the commonest cause of B12 deficiency and why?

A

Poor absorption of B12 – this is because the mechanism of absorption is complex, and can go wrong in many ways.

33
Q

What are the 2 methods of B12 absorption? - Which one is faster/efficient?

A

1: slow and inefficient (1%) – in the duodenum – direct absorption across intestinal wall.
2: B12 combines with intrinsic factor (made in parietal cells of the stomach. B12-IF binds to ileal receptors. Most absorption follows this route. Absorption still occurs in the small intestine

34
Q

What happens to B12 following absorption?

A

B12 is stored. When stores are saturated, excess B12 is excreted in the urine

35
Q

What are the 3 things needed for B12 absorption?

A
  1. An intact stomach
  2. A functioning small intestine
  3. Intrinsic factor
36
Q

Why may B12 deficiency be caused by intrinsic factor?

A
  • Post gastrectomy
  • Gastric atrophy
  • Antibodies to intrinsic factor or parietal cells (autoimmune disease)
  • Diseases of the small bowel (terminal ileum e.g. crohn’s disease, coeliac disease and surgical resection)
37
Q

What is pernicious anaemia?

Onset?
Family linked?
Females or males more dangerous in?

A
  • An autoimmune condition associated with a severe lack of intrinsic factor -> B12 deficiency
  • The peak age is 60 years – often associated with family history
  • Males have a slightly decreased life expectancy with PA, due to an increased risk of stomach cancer
38
Q

How should pernicious anaemia be diagnosed?

A

Look for intrinsic factor antibodies
(Occasionally found in other conditions, patients may not have intrinsic factor antibodies)

Look for parietal cell antibodies
( 90% adults with PA, 16% normal females over age of 60)

39
Q

Can parietal cell antibodies be used alone to diagnose pernicious anaemia and why?

A

You can get positive antibodies in patients who don’t have an illness (particularly in women above 50/60). The presence of antibodies on their own is not enough to definitely diagnose pernicious anaemia.

40
Q

Give examples of infections that can affect B12 levels

A
  • H Pylori
  • Giardia (intestinal parasite)
  • Fish tapeworm
  • Bacterial overgrowth
41
Q

What are some drugs associated with low B12?

A
  • Metformin (commonly used for diabetes and PCOS)
  • Proton pump inhibitors e.g. omeprazole
  • Oral contraceptive pill
42
Q

In patients with low B12, how should the cause be identified?

A
  • Check for antibodies to parietal cells and intrinsic factor and for antibodies for coeliac disease
  • Do a breath test for bacterial overgrowth
  • Check the stool for H Pylori
  • Test for Giardia
43
Q

What is the first thing that should be done in patients who are B12 deficient and how?

A
  • Treat the deficiency

- Replenish stores of B12 using injections

44
Q

What is the Shilling test and how is it done?

A
  • First deficiency is treated
  • Then you ask the patient to drink a radioactive sample of B12, and measure excretion in the urine
  • If someone is normal you would expect B12 to be in the urine (they have absorbed it and excreted)
  • If there is no B12 in the urine, it suggests that they cannot absorb B12
  • The test is repeated (drink radioactive B12 sample), with addition of intrinsic factor in the drink
  • Then you measure excretion of B12 in the urine – if B12 is present, the problem was with intrinsic factor
45
Q

What are some of the reasons for not seeing B12 in the urine in the shilling test?

A

Malabsorption of vitamin B12 (pernicious anaemia, small bowel disease), or no correction of B12 deficiency prior to the test.

46
Q

How is B12 deficiency treated?

What if the person has neurological involvement?

A
  • Injections of B12 (1000ug intramuscular)
  • 3 times a week for 2 weeks (6 injections in total over the 2 weeks)
  • Thereafter, give injections every 3 months
  • B12 injections are given more frequently: alternate days until no further improvement – up to 3 weeks
  • Thereafter every 2 months

Haematology (11 decks)

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