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Haematology > B12 and folate deficiencies > Flashcards

B12 and folate deficiencies Flashcards

1
Q

what is the role of both B12 and folate *

A

DNA synthesis

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2
Q

what is the effect of absence of B12 and folate *

A

severe anaemia - fatal

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3
Q

what is just B12 used for *

A

integrity of the nervous system

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4
Q

what is just folic acid used for *

A

homocystine metabolism

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5
Q

how are folate and B12 involved in dna synthesis *

A

dUMP (deoxy urinodine monophosphate) is converted to dTMP (deoxy thymidine monophosphate) by the transfer of a CH3 group - dTMP goes on to become DNA

dUMP gets the CH3 group from 5,10 methylene THF-polyglutamate

THf-polyglutamte becomes DHF polyglutamate when it gives up teh CH3

DHF glutamate is converted back to DHF glutamate but needs diety folate to be converted to THF whhich requires B12 - so need both folate and B12

folate also is involved in the conversion of homocystiene which is toxic to methionine

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6
Q

what is affected by B12 and phosphate *

A

all rapidly dividing cells:

bone marrow

epi cells of mouth and gut - produce lots of cells on daily basis)

gonads - spermatogeneis

embryos

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7
Q

what are symptoms of B12 and folate deficiency *

A

anaemia - weak, tired, short of breath

jaundice - break red cells down = increased BR

problems with GI tract - glossitis (inflammed tongue) and angular cheilosis (cracks in thecorner of mouth)

sterility in males

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8
Q

what are the 2 types of anaemia caused by B12 or folate acid deficiency *

A

(anaemia with a high MCV)

macrocytic

megaloblastic

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9
Q

what is macrocytic anaemia *

A

average red cell is above the normal range

descriptive term

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10
Q

causes of macrocytic anaemia *

A

vit B12/folate deficiency

liver disease/alcohol

hypothyroid

drugs eg azathroprine - immunosuppressant

haematological disorders - myelodysplasia, aplastic anaemia, reticulocytosis eg chronic haemolytic anaemia

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11
Q

what is megaloblastic anaemia *

A

describes a morphalogical change in teh red cell precursers within the bone marrow

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12
Q

what is the cause for megaloblastic anaemia *

A

b12 and folate deficiency

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13
Q

describe normal red cell maturation *

A

erythroblast - earliest recognisable form visually - nucleus and lots of proteins = blue

normoblast - early/intermediate/late - this depends on colour, cytoplasm gets more pink

nucleus gets smaller and pyknotic

reticulocyte - maybe some nucleic acid

circulating red blood cell - no nucleus and lots of hb

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14
Q

describe red cell maturation in megaloblastic anaemia *

A

asynchronus maturation of the nucleus and cutoplasm in the erythroid series

maturing red cells are seen in the bone marrow

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15
Q

what is present in the periperal blood in megaloblastic anaemia *

A

anisocytosis

large red cells

hypersegmented neutrophils - DNA production is affected

giant metamyelocytes

red cells have mature (red) cytoplasm but nucleus = immaturity in nucleus development

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16
Q

slide with asynchronus development of red cell *

A
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17
Q

describe hypersegmented neutrophil *

A

can tell neutrophil because hypersegmented

have >5 lobules

associated with megaloblastic change - ie folate or B12 deficiency

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18
Q

what tests would you do on someone with macrocytosis *

A

folate and B12

thyroid function test

liver function test

reticulocyte count - bigger than red cells

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19
Q

what is the dietry source of folate *

A

fresh leafy veg - destroyed by overcooking/canning/processing

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20
Q

2 causes of folate deficiency *

A

reduced intake

increased demand

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21
Q

wy would folate intake be reduced *

A

ignorance

poverty

apathy

eg in elderly and alcoholics - not going to eat leafy veg

22
Q

why would folate demand be increased *

A

physiological - pregnancy, adolescence, premature babies (because rapidly reproducing cells)

pathological - malignancy, erythroderma (large percentage of body inflammed), haemolytic anaemias (red cell production has to increase)

23
Q

when would you see folate deficiency *

A

alcoholic admitted with head injury after fight

30yr old lady with infected whole body eczema

90yr old who only eats jam sandwich

24
Q

how would you diagnose folate deficiency *

A

Fbc and film - raised MCV/megaloblastic signs

folate levels in serum (recent folate intake) or in red cells (indicates body stores of folate)

25
Q

how would you assess te cause of decreased folate *

A

history - diet/alcohol/illness

examination - skin disease/alcoholic liver disease

26
Q

what are the consequences of folate deficiency *

A

megaloblastic, macrocytic anaemia

neural tube defects in developing foetus

increased risk of thromosis - in association with variant enzymes involved in homocysteine metabolism - folate deficiency causes an increase in homocysteine

27
Q

describe neural tube defects from folate deficiency *

A

spina bifida -

anecepaly - born witout a brain

all pregnant women take folic acid 0.4mg prior to conception for at least 12 weeks

28
Q

describe how hhomocysteine is related to thrombosis *

A

very high levels of homocysteine (inborn error of metabolism) = atherosclerosis, premature vascular disease - very high rate of thrombosis

mildly elevated (when folate deficiency) = CVD definitely, arterial thrombosis probably, venous thrombosis possibly

29
Q

how has usa addressed folate defiency

A

fortify food with it

30
Q

what are the signs of B12 defiency *

A

parasthesiae - pins and needles

muscle weakness

difficulty walking

visual impairment

psychiatric disturbance

31
Q

what are consequences of B12 deficiency *

A

neurological problems - bilateral peripheral neuropathy, subacute combined degeneration of the cord (posterior and pyramidal tracts = paralysis), optic atrophy, dementia

affects the central and peripheral nervous system

can present in lots of ways

32
Q

what are classical clinical presentations of B12 deficiency *

A

parathesiae

low Hb,

high MCV

FH of autoimmune

glossitis

premature grey hair loss of proprioception

33
Q

what is romberg’s sign and wat does it test for *

A

for B12 defiency - loss of proprioception

stand, put hands out and close eyes

fall over because of loss of proprioception

34
Q

what would be seen in an examination for B12 deficiency *

A

absent reflexes - periperal nerve loss

upgoing plantar reflex - CNS damage

35
Q

what are the causes of B12 deficiency *

A

poor absorption - most common

reduced dietry intake - stores are large adn last for 3-4years, comes from diet, vegans at risk becasue on dairy

infections/infestations - they consume the B12 eg abnormnal bacterial flora (stagnant loops), tropical sprue, fish tapeworms

36
Q

describe normal B12 absorption *

A

occurs in SI - B12 stored - when stores are saturated B12 is excreted in the urine

2 methods:

1 - through the duodenum, slow and inefficient

2 - most this wayn - b12 combine wit intrinsic factor in SI, made by the parietal cells - B12-IF binds to ileal receptors and internalised

37
Q

what are the 3 things needed for most b12 absorption *

A

intact stomac - parietal cells

intrinsic factor

functioning small intestine

38
Q

what can cause impaired B12 absorption *

A

reduced IF

diseases of the small bowel (terminal ileum)

infection drugs

39
Q

how can IF be reduced *

A

post gastrectomy

gastric atrophy

Ab to IF or parietal cells - autoimmune

40
Q

what is pernicious anaemia *

A

autoimmune condition = severe lack of IF

peak age - 60yrs

have FH

male have decreased life expectancy because of stomach cancer

Have IF Ab (occaisionally found in other conditions)

parietal cell Ab - less specific, increase with age anyway doesnt mean you have pernicious anaemia

41
Q

what are diseases of the small bowel that affect b12 absorption *

A

crohns

coeliac

surgical resection

42
Q

what infections lead to B12 deficiency *

A

h pylori

giardia

fish tapeworm

bacterial overgrowth

43
Q

what drugs are associated with a low B12 *

A

metformin - for PCOS and diabetes

proton pump inhibitors eg omeprazole

oral contraceptive pill

44
Q

what investigations do you do to determine cause of B12 deficiency *

A

Ab to parietal cells and IF

Ab to coeliac disease

breath test - for bacterial overgrowth

stool for H pylori

test for giardia

used to do shilling test - cant do now because needs radioactivity

45
Q

what is the implication for treatment if you have B12 deficiency because of IF Ab *

A

cant give oral supplements - wont be able to absorb them

46
Q

describe the silling test *

A

prior to test restore the B12 stores (saturate the transcobalamin - these are B12 carrier proteins) - 6IM injections over 2 weeks when diagnosed to avoid neurological problems

drink radiolabled B12

measure excretion in urine

if in urine - means it has been absorbed into blood then filtered by kidney

if not in urine - not absorbed (pernicious anaemia, small bowel disease) - end up in stool, or hadnt corrected B12 before test - so not excreting it even though it is absorbed becasue it is just filling the stores

if not in urine repeat with IF using diff radioactive isotope - then measure B12 in urine - if now normal, problem is missing IF ie pernicious anaemia. - IF dependant malabsorption is course of B12 def

47
Q

what is the treatment for B12 deficiency *

A

injections of B12 - bypass the oral root

3 a week for 2 weeks

then every 3 months - stores last this long

if neurological involvement - b12 injections alternate days until no furter improvement up to 3 weeks – then every 2 months - some neurological things are irreversible

dont give IF to people with pernicious anaemia as ab will still attack it

48
Q

what test do you do if someone has low Hb and high MCV *

A

folate, b12, thyroid function, liver function

49
Q

where does absorption of folate occur *

A

duodenum and jejunum

50
Q

what is pancytopenia

A

low hb, leukocytes and platelets

51
Q

how do you manage folate deficiency *

A

diet

folate tablets daily

Haematology (11 decks)

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