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Haematology > IOD Microcytic and Macrocytic Anaemia > Flashcards

IOD Microcytic and Macrocytic Anaemia Flashcards

1
Q

History of iron deficiency anaemia?

A 
signs-tiredness, SOB
NSAIDs, steroids, anticoagulants
diet-vegan or veg
periods
bowel habits
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2
Q

Exam of iron deficiency anaemia?

A 
bruising
conjunctival pallor
angular stomatitis
pale mucosa
tachycardic
hypotensive
systolic flow murmur-increased CO/turbulent flow
kilonychia
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3
Q

Investigations?

A

FBC, iron and Hb, MCV, iron ,B12 and folate

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4
Q

FBC?

A

The most common blood test: used to assess number and size of cells found in blood

Often a ‘base line’ or ‘basic’ blood test

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5
Q

ETTA?

A

Stops clotting in vial so can be processed

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6
Q

Hb?

A

conc of Haemoglobin (g/L)

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7
Q

Hct

A

%of blood volume as RBC

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8
Q

MCV

A

Average size of RBC

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9
Q

MCH

A

Average haemoglobin content of RBC

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10
Q

MCHC

A

calculated measure of haemoglobin concentration in given red blood cells

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11
Q

RDW

A

_Range of deviation around RBC size

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12
Q

other FBC investigations?

A

Reticulocyte count

Blood film: microscopy

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13
Q

size?

A

big small normal

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14
Q

shape?

A 
fragments-microcytic haemolytic
tear drop-myelofibrosis
spiculated-sickle cell
ovalocyte-def, thalessaemia
spherocyte-spherocytosis
eliptocyte-elliptocytosis
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15
Q

colour?

A

pale normal, polychromatic (reticulocytes)

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16
Q

inclusions?

A

howell-jolly bodies (hyposplenism), nuclear remnants (thalessaemia), malarial parasites, basophilic stippling (lead poisoning)

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17
Q

microcytic features and causes?

A 
reduced MCV
small RBC
Iron deficiency 
(heme deficiency)
Thalassamia 
(globin deficiency)
Anaemia of Chronic Disease
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18
Q

Normocytic features and causes?

A 
normal MCV
normal RBC
Anaemia Chronic Disease-due to chronic condition
Aplasia-less synthesis
chronic renal failure
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19
Q

macrocytic features and causes?

A

B12 Deficiency
Folate Deficiency
myelodysplasia-abnormal cells
reticulocytosis-haemolysis-premature breakdown-high rbc turnover-blue centre-larger

drug induced-hydroxycarbamide-sickle and cancer-methotrexate-sodium valproate

Liver disease
hypothyroidism

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20
Q

what does reticulocyte count show?

A

failure of production or increased losses

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21
Q

Hb and MCV values in childhood and puberty?

A

13.5 g/dl to 9g/dl in 2 months and increases
as adaptation from hypoxic IU to well-oxygenated EU environment
MCV decreases from birth to 1 yr and increase in puberty
males-high hb-effects of androgens on erythropoiesis

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22
Q

Iron?

A

Essential for O2 transport
Most abundant trace element in body

Daily requirement for iron for erythropoeisis varies depending on gender and physiolgical needs

23
Q

Daily iron requirements

A

higher when child
higher for women if pre-menopausal, preg of BF
Recommended intake assumes 75% of iron is from heme iron sources (meats, seafood). Non-heme iron absorption is lower for those consuming vegetarian diets, for whom iron requirement is approximately 2-fold greater.

24
Q

Iron metabolism?

A

> 1 stable form of iron:
Ferric states (3+) and Ferrous states (2+)
Most iron is in body as circulating Hb
ferrous has a higher bioavailability-haem form-in meats-absorbed more

Hb: 4 haem groups, 4 globin chains able to bind 4 O2

Remainder as storage and transport proteins
ferritin and haemosiderin (high is sickle cell or thalessaemia)
Found in cells of liver, spleen and bone marrow

25
Q

Absorption transprt adn storage of iron?

A

Iron is absorbed from duodenum via enterocytes into plasma and binds to transferrin and then transported to bone marrow to make red blood cells

Excess absorption of iron is stored as ferritin

Regulated by GI mucosal cells mechanism: max absorption in duodenum & proximal jejunum via ferroportin receptors

Amount absorbed depends on type ingested
heme, ferrous (red meat, used to contain haemoglobin)
non-heme, ferric forms which is bound to other substances.
Heme iron makes up 10-20% of dietary iron

Other foods, GI acidity, state of iron storage levels and bone marrow activity affect absorption

26
Q

Distribution of iron?

A

duodenum enterocytes absorb iron and binds to plasma transferrin
used my muscle myoglobin and bone marrow
stored in liver Hb and Reticuloendothelial macrophages
- ingest senescent red cells, catabolise haemoglobin to scavenge iron, and load the iron onto transferrin for reuse.

Iron metabolism is unusual in that it is controlled by absorption rather than excretion. Iron is only lost through blood loss or loss of cells as they slough.
Men and nonmenstruating women lose about 1 mg of iron per day. Menstruating women lose from 0.6 to 2.5 percent more per day.

An average 60-kg woman might lose an extra 10 mg of iron per menstruation cycle, but the loss could be more than 42 mg per cycle depending on how heavily she menstruates.

27
Q

hepcidin?

A

“ the iron-regulatory hormone hepcidin and its receptor and iron channel ferroportin control the dietary absorption, storage, and tissue distribution of iron…

Hepcidin causes ferroportin internalization and degradation, thereby decreasing iron transfer into blood plasma from the duodenum, from macrophages involved in recycling senescent erythrocytes, and from iron-storing hepatocytes.
Hepcidin is feedback regulated by iron concentrations in plasma and the liver and by erythropoietic demand for iron.”

28
Q

serum Fe?

A

variable during the day-low if iron def

29
Q

ferritin?

A

primary storage protein and providing reserve-water soluble-low in iron def

30
Q

transferrin stas?

A

ratio of serum iron and total iron binding capacity-% occupancy
low in iron def

31
Q

total iron binding capacity?

A

capacity of transferrin to bind to iron-indirectly measures transferrin
high in iron def

32
Q

stages in development of IDA?

A

Before anaemia develops, iron deficiency occurs in several stages.
Serum ferritin is the most sensitive laboratory indicators of mild iron deficiency. Stainable iron in tissue stores is equally sensitive, but is not performed in clinical practice.-gold standard-bone marrow biopsy-staining-invasive and time consuming
The percentage saturation of transferrin with iron and free erythrocyte protoporphyrin values do not become abnormal until tissue stores are depleted of iron.
A decrease in the haemoglobin concentration occurs when iron is unavailable for haem synthesis.
MCV and MCH do not become abnormal for several months after tissue stores are depleted of iron.

33
Q

Causes of iron def?

A 
NOT ENOUGH IN
Poor Diet
Malabsorption
Increased physiological needs
LOSING TOO MUCH
Blood loss
menstruation, GI tract loss, parasites
34
Q

results of IDA?

A 
Anaemic
Microcytic
Low reticulocyte
Low production
Low iron
low Ferritin
High transferrin
Low iron sats
35
Q

IDA blood film?

A 
Ansiocytosis-abnormal cell size
Poikilocytosis-abnormal shape
Elliptocytes
Hypochromia-less pigment
Microcytosis
Size-compare to lymphocyte
36
Q

IDA management?

A

Refer to gynae, iron supplements (constipation) oral or iv, dietary, Iv acts quicker, transfusion if severe

37
Q

is iron def a diagnosis?

A

No-always try to find cause of this!

38
Q

Thalessaemia?

A

low MCV, high ferritin low Hb
shows globin def not haem def
iron therapy doesn’t work

39
Q

macrocytosis low reticulocyte count?

A

Vitamin B12/Folic acid deficiency
Drug-related
(interference with B12/FA metabolism-methotrexate and folate)

40
Q

macrocytosis nonmegaloblastic?

A 
Alcoholism ++
Hypothyroidism
Liver disease
Myelodysplastic syndromes
Reticulocytosis (haemolysis)
41
Q

megaloblastic?

A

Megaloblastic changes of blood cells are seen in B12 and Folic Acid deficiency. They are characterized on the peripheral smear by macroovalocytes and hypersegmented neutrophils.

42
Q

folate uses?

A

DNA synthesis-AGT

43
Q

causes of folate def?

A

increased demand?
decreased intake?
decreased absorption?

44
Q

increased demand?

A 
preg/bf
infancy ad growth spurts
heamolysis and rapid cell turnover
disseminated cancer
urinary losses-HF
45
Q

decreased intake?

A

poor diet
elderly
chronic alcohol intake

46
Q

decreased absorption?

A

medication
coeliac
jejunal resection
tropical sprue

47
Q

vit B12?

A

Essential co-factor for methylation in DNA and cell metabolism

Intracellular conversion to 2 active coenzymes necessary for the homeostasis of methylmalonic acid (MMA) and homocysteine and methionine
mma checked as b12 not sensitive

48
Q

foods with B12?

A

Foods containing vit B12:
Animal sources: Fish, meat, dairy

UK intake recommendations are 1.5mcg/day
EU: 1mcg/day and USA: 2.4mcg/day
average western intake 5-30mcg/day
Body (liver) storage: 1-5mg so many years for deficiency

49
Q

What is needed for Vit B12 absorption?

A

Requires the presence of Intrinsic Factor for absoprtion in terminal ileum

IF made in Parietal Cells in stomach
Transcobalamin II and Transcobalamin I transport vitB12 to tissues

50
Q

causes of VitB12 deficiency?

A

impaired absorption-pernicious anaemia
gastrectomy or ileal resection
ZE syndrome
parasites

Decreased intake-malnutrition and vegan diet

congenital causes-
IFR def or cobalamin mutation CG1 gene

increased needs-haemolysis, HIV,PREG growth spurts

meds
alcohol-folate def more and poor diet
NO
PPI/H2A
metformin
51
Q

haematological effects of VitB12 def?

A

MCV normal or high-Megaloblastic anaemia
Ineffective erythropoeisis
Hb-normal or low
reticulocyte count-low
LDH(lactate dehydrogenase)-raised-IM haemolysis or malignancy
blood film-macrocytes, ovalocytes, hypersegmented neuts
BMAT-Hypercellular, megaloblastic, giant metamyelocytes-unusual
MMA-highly sensitive-increased-not standard lab test-highly sensitive

52
Q

effects of VitB12 def?

A 
Brain: cognition, depression, psychosis
Neurology: 
myelopathy, sensory changes, ataxia, spasticity (SC columns degeneration)
(SACDC)
Infertility
Cardiac cardiomyopathy
Tongue: glossitis, taste impairment
Blood: Pancytopenia
53
Q

Pernicious Anaemia?

A

Autoimmune disorder
Lack of IF
Lack of
B12 absorption

Gastric Parietal cell antibodies
IF antibodies
test for ABs and give B12 injections-twice for 2 weeks and once every 3 months

Haematology (4 decks)

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