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Y2 MCD Haematology > haemoglobin > Flashcards

haemoglobin Flashcards

B12 and folate: explain the role of vitamin B12 and folic acid in haemopoiesis and biochemical pathways; recall dietary sources, mechanisms of absorption, and causes of deficiency; explain the clinical features, haematological features, diagnosis, investigation and management of these deficiencies

1
Q

cause of neutrophil hypersegmentation

A

lack of vitamin B12 or folic acid

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2
Q

cause of megaloblastic anaemia

A

lack of vitamin B12 or folic acid

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3
Q

roles of vitamin B12 and folate

A

required for DNA synthesis

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4
Q

what can absence of vitamin B12 and folate lead to

A

severe anaemia, which can be fatal

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5
Q

what is vitamin B12 requied for

A

DNA synthesis, integrity of nervous system

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6
Q

what is folic acid required for

A

DNA synthesis, homocystine metabolism

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7
Q

in DNA synthesis, what are vitamin B12 and folate required for; diagram

A

production of deoxythmidine (made from deoxyuridine)

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8
Q

what rapidly dividing cells are affected in vitamin B12 and folate deficiency

A

all: bone marrow, epithelial surfaces of mouth and gut, gonads, embryos

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9
Q

5 clinical features of vitamin B12 and folate deficiency

A

anaemia so weak, tired and short of breath; jaundice (increased bilirubin production); glossitis and angular cheilosis; weight loss, change of bowel habit; sterility (esp. males)

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10
Q

what type of anaemia is present in vitamin B12 and folate deficiency

A

macrocytic and megaloblastic

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11
Q

define macrocytic

A

average red cell MCV above normal range

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12
Q

5 causes of macrocytic anaemia

A

vitamin B12 and folate deficiency, liver disease (affects production of red cell proteins) or alcohol, hypothyroid, drugs e.g. azathioprine (immunosuppressant), haematological disorders

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13
Q

3 haematological disorders causing macrocytic anaemia

A

myelodysplasia, aplastic anaemia, reticulocytosis e.g. chronic haemolytic anaemia

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14
Q

define megaloblastic

A

morphological change in red cell precursors within bone marrow; only in folate and B12 deficiency

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15
Q

normal red cell maturation

A

erythroblast -> normoblast (early/intermediate/late) -> reticulocyte -> circulating red blood cell

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16
Q

red cell development diagram (end to beginning): mature red cell, reticulocyte, pyknotic erythroblast, polychromatic erythroblast, basophilic erythroblast, proerythroblast

A

diagram

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17
Q

define megaloblastic anaemia

A

asynchronous maturation of nucleus and cytoplasm in erythroid series, with maturing red cells seen in bone marrow e.g. nucleus still present in mature cytoplasm

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18
Q

4 aspects of peripheral blood in megaloblastic anaemia

A

anisocytosis, large red cells, hypersegmented neutrophils (granules in cytoplasm; nucleus with more than 5 segments is abnormal), giant metamyelocytes

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19
Q

3 tests if someone had macrocytosis

A

folate and vitamin B12, thyroid function test, liver function test, reticulocyte test (if high, higher MCV)

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20
Q

what to check if see hypersegmented neutrophil

A

folate and vitamin B12 as indicates megaloblastic anaemia

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21
Q

where is dietary folate present in diet, and how is it destroyed

A

fresh, leafy vegetables; destroyed in overcooking, canning, processing

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22
Q

folate deficiency presentation

A

alcholic, trauma, infected whole body eczema, elderly with unvaried diet

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23
Q

causes of decreased folate intake

A

ignorance, poverty, apathy; e.g. elderly, alcoholics

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24
Q

3 causes of increased physiological demand of folate

A

pregnancy, adolescence, premature babies

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25
3 causes of increased pathological demand of folate
malignancy, erythoderma (large propotion of red skin due to inflammatory disease), haemolytic anaemias
26
2 methods of laboratory diagnosis of folate deficiency
FBC and film, folate levels in blood
27
how is cause of decreased folate assessed
history (diet, alcohol, illness), examination (skin disease, alcoholic liver disease)
28
3 consequences of folate deficiency
megaloblastic, macrocytic anaemia; exacerbate neural tube defects in developing foetus; increased risk of thrombosis in association with variant enzymes involved in homocysteine metabolism
29
2 neural tube defects caused by folate deficiency
spina bifida, anencephaly
30
how is folate deficiency avoided in pregnant women
take folic acid 0.4mg prior to conception and for first 12 weeks
31
what are very high levels of homocysteine associated with
atherosclerosis, premature vascular disease
32
what are mildly elevated levels of homocysteine associated with
definitely CVD, probably arterial thrombosis, possible venous thrombosis
33
in USA how is folate deficiency attempted to be avoided
grains fortified with folic acid
34
B12 deficiency presentation and history
paraesthesiae, low Hb, high MCV, history of auto-immune disease, low B12, glossitis, premature grey hair, muscle weakness, difficulty walking, visual impairment, psychiatric disturbance, Romberg's sign
35
what is Romberg's sign
loss of proprioception and fall over when close eyes
36
neurological problems as a consequence of vitamin B12 deficiency
bilateral peripheral neuropathy, subacute combined degeneration of cord (posterior and pyramidal tracts), optic atrophy, dementia
37
B12 deficiency examination
absent reflexes and upgoing plantar responses (CNS and ANS nerve damage)
38
3 causes of vitamin B12 deficiency
poor absorption, reduced dietary intake, infections/infestations
39
reduced dietary intake as cause of vitamin B12 deficiency
stores are large (last for 3-4 years), animal produce, vegans at risk (must take B12 supplements)
40
infections/infestations as cause of vitamin B12 deficiency
abnormal bacterial flora (stagnant loops), tropical sprue, fish tapeworm
41
where does normal vitamin B12 absorption occur, and fate
in small intestine, whete it is then stored until saturation, with excess B12 excreted in urine
42
2 methods of absorption of B12
method 1: slow and inefficient, duodenum; method 2: most absorption, B12 must combine with intrinsic factor (made in patietal cells of stomach), with B12-IF binding to ileal receptors
43
3 things essential for B12 absorption
intact stomach, intrinsic factor, functioning small intestine
44
3 things responsible for intrinsic factor reduction causing impaired B12 absorption
post gastectomy, gastric atrophy, antibodies to intrinsic factor or parietal cells
45
define pernicious anaemia; peak age and inheritance
autoimmune condition associated with severe lack of intrinsic factor; peak age at 60 years, family history
46
male life expectancy in pernicious anaemia and why
males have decreased life expectancy (stomach cancer)
47
when are intrinsic factor antibodies found
in pernicious anaemia and occasionally other conditions
48
when are parietal cell antibodies found
most adults with pernicious anaemia, some normal females >60, increased in relative of patients with pernicious anaemia
49
3 diseases of small bowel (terminal ileum) causing impaired B12 absorption
Crohns, coeliac disease, surgical resection
50
4 infections causing impaired B12 absorption
H Pylori, Giardia, fish tapeworm, bacterial overgrowth
51
3 drugs associated with low B12
metformin (type 2 diabetes, polycystic ovarian syndrome), proton pump inhibitors e.g. omeprazole (indigestion, reduced stomach acid secretion), oral contraceptive pill
52
how to determine cause of B12 deficiency
antibodies to parietal cells and intrinsic factor, antibodies for coeliac disease, breath test for bacterial overgrowth, stool for H Pylori, test for Giardia; before was Shilling test to determine if oral (fine absorption) or injection (abnormal absorption e.g. pernicious anaemia)
53
determining cause of B12 deficiency: Shilling test part 1
prior to test, replenish stores; drink radiolabelled B12 and measure excretion in urine - if not present then something wrong
54
possibilities of no radiolabelled B12 in urine after Shilling test part 1
not absorbing B12 so will come out in faeces (pernicious anaemia, small bowel disease), hadn't corrected B12 deficiency before test so not excreting it
55
determining cause of B12 deficiency: Shilling test part 2 to determine why not absorbing B12
repeat test but B12 bound to intrinsic factor (different isotope), measure excretion of B12 in urine
56
outcome if Shilling test part 1 low and 2 normal
no instrinsic factor production
57
outcome if Shilling test part 1 low and 2 also low
no issue with intrinsic factor (so stomach or small intestine not functioning correctly)
58
if classic case but normal B12, what should be measured, and how should it be treated
measure methylmalonyl acid, homocysteine, look for anti-intrinsic factor antibodies; treat as B12 deficiency until results back
59
treatment of B12 deficiency
1000ug i.m. injections of B12 3x/week for 2 weeks, then thereafter every 3 months
60
treatment of B12 deficiency if neurological involvement
B12 injections alternate days until no further improvement up to 3 weeks, then thereafter every 2 months

Y2 MCD Haematology (20 decks)

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