Brainscape's Knowledge GenomeTM

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


See full index

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

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

cause of megaloblastic anaemia

A

lack of vitamin B12 or folic acid

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

roles of vitamin B12 and folate

A

required for DNA synthesis

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

what can absence of vitamin B12 and folate lead to

A

severe anaemia, which can be fatal

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

what is vitamin B12 requied for

A

DNA synthesis, integrity of nervous system

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

what is folic acid required for

A

DNA synthesis, homocystine metabolism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

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

A

production of deoxythmidine (made from deoxyuridine)

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

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

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

A

macrocytic and megaloblastic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

define macrocytic

A

average red cell MCV above normal range

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

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

3 haematological disorders causing macrocytic anaemia

A

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

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

define megaloblastic

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

normal red cell maturation

A

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

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

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

A

diagram

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

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

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what to check if see hypersegmented neutrophil

A

folate and vitamin B12 as indicates megaloblastic anaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

folate deficiency presentation

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

causes of decreased folate intake

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

3 causes of increased physiological demand of folate

A

pregnancy, adolescence, premature babies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

3 causes of increased pathological demand of folate

A

malignancy, erythoderma (large propotion of red skin due to inflammatory disease), haemolytic anaemias

26
Q

2 methods of laboratory diagnosis of folate deficiency

A

FBC and film, folate levels in blood

27
Q

how is cause of decreased folate assessed

A

history (diet, alcohol, illness), examination (skin disease, alcoholic liver disease)

28
Q

3 consequences of folate deficiency

A

megaloblastic, macrocytic anaemia; exacerbate neural tube defects in developing foetus; increased risk of thrombosis in association with variant enzymes involved in homocysteine metabolism

29
Q

2 neural tube defects caused by folate deficiency

A

spina bifida, anencephaly

30
Q

how is folate deficiency avoided in pregnant women

A

take folic acid 0.4mg prior to conception and for first 12 weeks

31
Q

what are very high levels of homocysteine associated with

A

atherosclerosis, premature vascular disease

32
Q

what are mildly elevated levels of homocysteine associated with

A

definitely CVD, probably arterial thrombosis, possible venous thrombosis

33
Q

in USA how is folate deficiency attempted to be avoided

A

grains fortified with folic acid

34
Q

B12 deficiency presentation and history

A

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
Q

what is Romberg’s sign

A

loss of proprioception and fall over when close eyes

36
Q

neurological problems as a consequence of vitamin B12 deficiency

A

bilateral peripheral neuropathy, subacute combined degeneration of cord (posterior and pyramidal tracts), optic atrophy, dementia

37
Q

B12 deficiency examination

A

absent reflexes and upgoing plantar responses (CNS and ANS nerve damage)

38
Q

3 causes of vitamin B12 deficiency

A

poor absorption, reduced dietary intake, infections/infestations

39
Q

reduced dietary intake as cause of vitamin B12 deficiency

A

stores are large (last for 3-4 years), animal produce, vegans at risk (must take B12 supplements)

40
Q

infections/infestations as cause of vitamin B12 deficiency

A

abnormal bacterial flora (stagnant loops), tropical sprue, fish tapeworm

41
Q

where does normal vitamin B12 absorption occur, and fate

A

in small intestine, whete it is then stored until saturation, with excess B12 excreted in urine

42
Q

2 methods of absorption of B12

A

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
Q

3 things essential for B12 absorption

A

intact stomach, intrinsic factor, functioning small intestine

44
Q

3 things responsible for intrinsic factor reduction causing impaired B12 absorption

A

post gastectomy, gastric atrophy, antibodies to intrinsic factor or parietal cells

45
Q

define pernicious anaemia; peak age and inheritance

A

autoimmune condition associated with severe lack of intrinsic factor; peak age at 60 years, family history

46
Q

male life expectancy in pernicious anaemia and why

A

males have decreased life expectancy (stomach cancer)

47
Q

when are intrinsic factor antibodies found

A

in pernicious anaemia and occasionally other conditions

48
Q

when are parietal cell antibodies found

A

most adults with pernicious anaemia, some normal females >60, increased in relative of patients with pernicious anaemia

49
Q

3 diseases of small bowel (terminal ileum) causing impaired B12 absorption

A

Crohns, coeliac disease, surgical resection

50
Q

4 infections causing impaired B12 absorption

A

H Pylori, Giardia, fish tapeworm, bacterial overgrowth

51
Q

3 drugs associated with low B12

A

metformin (type 2 diabetes, polycystic ovarian syndrome), proton pump inhibitors e.g. omeprazole (indigestion, reduced stomach acid secretion), oral contraceptive pill

52
Q

how to determine cause of B12 deficiency

A

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
Q

determining cause of B12 deficiency: Shilling test part 1

A

prior to test, replenish stores; drink radiolabelled B12 and measure excretion in urine - if not present then something wrong

54
Q

possibilities of no radiolabelled B12 in urine after Shilling test part 1

A

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
Q

determining cause of B12 deficiency: Shilling test part 2 to determine why not absorbing B12

A

repeat test but B12 bound to intrinsic factor (different isotope), measure excretion of B12 in urine

56
Q

outcome if Shilling test part 1 low and 2 normal

A

no instrinsic factor production

57
Q

outcome if Shilling test part 1 low and 2 also low

A

no issue with intrinsic factor (so stomach or small intestine not functioning correctly)

58
Q

if classic case but normal B12, what should be measured, and how should it be treated

A

measure methylmalonyl acid, homocysteine, look for anti-intrinsic factor antibodies; treat as B12 deficiency until results back

59
Q

treatment of B12 deficiency

A

1000ug i.m. injections of B12 3x/week for 2 weeks, then thereafter every 3 months

60
Q

treatment of B12 deficiency if neurological involvement

A

B12 injections alternate days until no further improvement up to 3 weeks, then thereafter every 2 months

Y2 MCD Haematology (20 decks)

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