Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Haematology > 10. Vitamin B12 and folic acid deficiency > Flashcards

10. Vitamin B12 and folic acid deficiency Flashcards

1
Q

What are haematinics?

A
  • Vitamins and minerals required for normal erythropoiesis

* Iron, B12 and folate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is vitamin B12 and folate generally required for?

A

B12
• DNA synthesis
• Integrity of the nervous system - CNS and PNS

Folate
• DNA synthesis
• Homocysteine metabolism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How does B12 and folate contribute to DNA synthesis?

A

• Deoxyuridine => deoxythymidine
- addition of methyl group
- this methylation requires the conversion of folate to different forms
- one of these steps also requires B12 (cofactor)
• Deoxythymidine = thymidine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the clinical features of B12/folate deficiency?

A
  • All rapidly dividing cells affected
  • Worse effects in bone marrow, epithelial surfaces of the GIT, gonads and embryogenesis
  • Anaemia - weakness, shortness of breath
  • Glossitis, angular cheilosis
  • Weight loss, change of bowel habit
  • Sterility may occur
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What types of anaemia can B12/folate deficiency result in?

A
  • Macrocytic - high MCV, large and macrocytic cells

* Megaloblastic - morphological change in red cell precursors within bone marrow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the causes of macrocytic anaemia?

A
  • Vitamin B12/folate deficiency
  • Liver disease or alcohol
  • Hypothyroidism
  • Drugs e.g. azathioprine (immunosuppressant)
  • Haematological disorders e.g. reticulocytosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How does the nucleus and cytoplasm of a red cell change during maturation?

A
  • Nucleus gets smaller - until pyknotic (irreversible condensation of chromatin)
  • Cytoplasm gets more pink due to haemoglobin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What happens during maturation in megaloblastic anaemia?

A
  • DNA not produced normally
  • Asynchronous maturation of the nucleus and cytoplasm
  • Cells with blue cytoplasm and no nucleus, or pink cells with a nucleus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What can be observed in the peripheral blood in megaloblastic anaemia?

A
  • Anisocytosis (red cells of unequal size)
  • Large red cells
  • Hypersegmented neutrophils
  • Giant metamyelocytes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Where can folate be found in the diet and where is folate deficiency seen?

A
  • Found in fresh or frozen leafy vegetables
  • Can be destroyed by overcooking/canning/processing
  • Deficiency can be caused by decreased intake: ignorance, poverty, apathy
  • Deficiency often seen in the elderly and alcoholics
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

When does an increased demand in folate tend to occur (physiological and pathological)?

A
  • Physiological - pregnancy, adolescence, premature babies

* Pathological - malignancy, erythroderma, haemolytic anaemias

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How can you diagnose folate deficiency in the lab?

A
  • Full blood count and blood film

* Serum folate levels in blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How can you assess the cause of folate deficiency?

A
  • Take a history: diet, alcohol, illness

* Examination: skin disease, alcoholic liver disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the consequences of folate deficiency?

A
  • Megaloblastic, macrocytic anaemia
  • Neural tube defects in developing foetus
  • Increased risk of thrombosis (in association with variant enzymes involved in homocysteine metabolism)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What neural tube defects can folate deficiency lead to in pregnancy and how can this be avoided?

A
  • Spina bifida and anencephaly

* Take 0.4mg folic acid prior to conception and for the first 12 weeks of pregnancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the link with homocysteine, folate/B12 and thrombosis?

A
  • Step in folate pathway that involves B12, in which homocysteine => methionine
  • Both essential amino acids
  • Homocysteine is toxic
  • Very high homocysteine levels are associated with atherosclerosis and premature vascular disease
17
Q

What are mildly elevated levels of homocysteine associated with?

A
  • Cardiovascular disease (definite)
  • Arterial thrombosis
  • Venous thrombosis
18
Q

What are the neurological consequences of B12 deficiency?

A
  • Bilateral peripheral neuropathy
  • Subacute combine degeneration (SCD) of the spinal cord (posterior and pyramidal tracts)
  • Optic atrophy
  • Dementia
19
Q

What type of history can you expect from a patient with B12 deficiency?

A
  • Paraesthesiae
  • Muscle weakness
  • Difficulty walking
  • Visual impairment
  • Psychiatric disturbance
20
Q

What motor neurone signs can you see in someone with B12 deficiency?

A
  • Upper and lower motor neurone signs
  • Reflexes may be absent (peripheral neuropathy)
  • Upgoing plantar response (Babinski’s sign) - upper motor neurone lesion sign
21
Q

What are the causes of B12 deficiency?

A 
• Poor absorption (most common)
• Reduced dietary intake
- stores last 3-4 years
- B12 found in all animal produce
- vegans at risk
• Infections (can consume B12)
- abnormal bacterial flora
- H. Pylori
- fish tapework
• Drugs
22
Q

What are the 2 methods of B12 absorption?

A

1) In duodenum, slow and inefficient (1%), direct absorption across intestinal wall
2) B12 combines with intrinsic factor (made by parietal cells of stomach). B12-IF binds to ileal receptors (most absorption)

Excess B12 excreted in urine when stores are saturated

23
Q

What 3 things does B12 absorption require?

A
  • Intact stomach
  • Functioning small intestine
  • Intrinsic factor
24
Q

What is pernicious anaemia?

A
  • Autoimmune condition
  • Severe lack of intrinsic factor
  • Leads to B12 deficiency
  • Peak age is 60 years
  • Associated with family history
  • Men have slightly decreased life expectancy due to increased risk of stomach cancer
25
Q

When should you look out for GI malignancy in someone with B12 deficiency?

A

If they develop iron deficiency

26
Q

Which antibodies should you look out for in pernicious anaemia?

A
  • Intrinsic factor antibodies
  • Parietal cell antibodies (90% of adults with PA, 16% normal female over 60yrs)

Antibodies are not enough to make a diagnosis

27
Q

Which drugs are associated with low B12?

A
  • Metformin
  • Proton pump inhibitors
  • Oral contraceptive pill
28
Q

What tests can you do to identify the cause of B12 deficiency?

A
  • Check for antibodies to IF, parietal cells and coeliac disease
  • Breath test for bacterial overgrowth
  • Check stool for H. Pylori
  • Test for Giardia
29
Q

What is the Schilling test?

A
  • Treat the deficiency first - replenish B12 stores using injection and capsules
  • Ask patient to drink radioactive B12
  • Measure excretion in urine
  • Normally there should be B12 present
  • No B12 - suggests it cannot be absorbed or B12 hasn’t been corrected prior to the test
30
Q

What are the new tests for B12 deficiency?

A
  • Plasma homocysteine (high in B12 and folate deficiency)
  • Serume Methylmalonic acid levels (expensive)
  • Holotransconbalamin levels (immunoassay - measures active B12)
31
Q

What is the treatment for B12 deficiency?

A
  • Injections of B12 (1000μg IM)
  • 3 times a week for 2 weeks
  • Once every 3 months thereafter
  • More often if patient has neurological involvement

Haematology (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions