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MCD Haematology > Iron Deficiency and Anaemic of Chronic Disease > Flashcards

Iron Deficiency and Anaemic of Chronic Disease Flashcards

1
Q

how is most iron in the body found as?

A

Hb

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2
Q

what sort of iron is found in HB?

A

ferrous in the haem part
role of holding onto oxygen

haem is made of a protoporphyin ring with an iron atom in the centre

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3
Q

how much iron needs to be consumed daily to replace the loss of red cells?

A

20 mg

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4
Q

how is iron lost by the body?

A

desquamated cells of the skin and gut

bleeding (menstruation)

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5
Q

where in the diet can iron be found?

A 
red meat 
offal
fish 
vegetables
whole grain cereal 
chocolate
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6
Q

how much iron is lost by men and women per day?

A

men: ~1mg a day
women: ~2mg a day

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7
Q

why is most consumed iron not absorbed?

A 
the body can not absorb Fe3+ (ferric) 
only ferrous (Fe2+) is absorbed

haem is better absorbed than free iron in general (10% compared to 1-2%)

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8
Q

what drink can enhance Fe2+ absorption?

A

orange juice (acid pH, ascorbic acid)

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9
Q

what drink can decrease Fe2+ absorption?

A

tea (alkaline pH, phytates and phosphates)

it converts iron to its ferric form and can lead to chronic low levels of ferrous

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10
Q

what are the3 factors that affect the absorption of iron?

A 
diet 
intestine (acid) 
systemic (iron def)
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11
Q

what 3 things lead to an increase in iron absorption?

A
  • iron deficiency
  • anaemia/hypoxia
  • pregnancy
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12
Q

what protein facilities the transport of iron into the blood?

A

ferroportin

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13
Q

which molecule inhibits the channel transporting iron into the blood?

A

hepcidin inhibits ferroportin

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14
Q

where can ferroportin be found?

A

enterocytes of duodenum
macrophages of the spleen
hepatocytes

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15
Q

what is iron from the diet (in the lumen) converted to intracellularly?

A

ferritin

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16
Q

how is the newly produced ferritin carried in the blood?

A

bound to transferrin in the plasma

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17
Q

where is transferrin produced?

what is normal transferrin saturation with iron?

A

produced in the liver (glycoprotein)

20-40%

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18
Q

what are the 3 measurements made with iron?

A

Total Iron Binding capacity (TIBC)
Transferrin Saturation
Transferrin Level

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19
Q

how is iron absorbed at the site required?

A

as transferrin cannot enter directly, it binds to the Tf-R and is taken up altogether

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20
Q

when is iron released by transferrin when endoctyosed as a complex?

A

with a drop in pH

transferrin receptors can be recycled at this point

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21
Q

what is the purpose of iron binding to transferrin?

A

iron is toxic and insoluble

there is no excretion system for iron

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22
Q

where is EPO produced?

A

kidneys

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23
Q

in response to what is EPO production increased?

A

hypoxia triggering more RBC precursors to be releases

these precursors survive longer and will eventually grow and differentiate

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24
Q

in which patients is ACD seen?

A

in patients with chronic disease

they dont show the classic causes of anaemia (no obvious cause)

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25
what are the lab signs of ACD?
o Higher levels of C-reactive protein – an acute phase protein (inflammation/infection). o Higher Erythrocyte Sedimentation Rate (ESR) – rises in inflammation/infection. o An acute phase response and increases in: ferritin, Factor VIII, fibrinogen and IG. i.e. high CRP, high ESR indicate ACD
26
what conditions are associated with ACD?
o Chronic infections – e.g. TB/HIV. o Chronic inflammation. o Malignancy. o Misc. – e.g. cardiac failure.
27
what is the main pathogenesis mechanism of ACD
cytokine release TNF alpha and IL interference with iron transport
28
how do cytokines lead to ACD?
- prevent usual flow of iron from the duodenum to the red cells i.e. block iron utilisation - stop EP increase - increase ferritin production - increase RBC death therefore reduced RBC production, and less iron available cytokines affect iron transport
29
what is the major cause of iron def?
blood | bleeding e.g. menstrual or GI bleed
30
what are the minor causes of iron def?
- increase use of iron e.g. pregnancy/ growth - dietary def e.g. vegetarian - malabsorption e.g. coeliac disease
31
when are full GI investigations carried out for iron def?
- males - women over 40, post-menopausal - woman with scanty menstrual loss
32
what makes up a full GI investigation ?
upper GI endoscopy (oesophagus, stomach, duodenum) duodenal biopsy colonoscopy if nothing is found a small bowel meal is given
33
when is no investigation done?
- a menstruating women <40 with heavy periods - multiple pregnancies - no GI symptoms
34
what also can be investigated to find the cause of iron def?
urinary blood loss (renal tract) antibodies for coeliac disease bleeding cancers (chronic, low grade)
35
what are the lab parameters in blood tests that would be useful in investigation?
- serum iron - total iron binding capacity - transferrin saturation - serum ferritin - haemosiderin in bone marrow using Prussian blue solution - MCV
36
causes of low MCV [3]
iron def thalassemia trait ACD
37
serum levels in the causes of low MCV
iron def has low serum Fe ACD has low serum Fe thala. trait has normal Fe
38
ferritin levels in the causes of low MCV
iron def has low ferritin | ACD has high ferritin (due to interfered transportation, nothing is moved from ferritin)
39
why is ferritin not reliable in telling whether someone has iron def?
it could also mean they have underlying ACD (high ferritin level) e.g. RA with bleeding ulcer a raised CRP and ESR would indicate an underlying condition
40
transferrin levels in the causes of low MCV
- iron def has a transferrin increase (attempt to use) | - ACD has normal or low transferrin (little transport)
41
transferrin saturations in causes of low MCV
- iron def has low transferrin sat (more transferrin, less iron) - ACD has normal transferring sat (iron and transferrin both decrease so sat is normal)
42
further investigation to blood test
```  Endoscopy and colonoscopy.  Duodenal biopsy.  Anti-helicobacter antibodies.  Anti-coeliac antibodies.  Other – abdominal ultrasound to look at kidneys, dipstick urine, pelvic US to exclude fibrosis. ```
43
thalassemia trait parameter results: serum iron- ferritin- TIBC- (same as transferrin level)
serum iron- NORMAL ferritin- NORMAL TIBC- NORMAL Hb- LOW MCV- LOW transferrin- NORMAL transferrin sat- NORMAL
44
classic ACD parameter results: serum iron- ferritin- TIBC- (same as transferrin level)
serum iron- LOW ferritin- HIGH OR NORMAL TIBC- NORMAL OR LOW Hb- LOW MCV- LOW OR NORMAL transferrin- NORMAL OR LOW transferrin sat- NORMAL
45
classic iron def parameter results: serum iron- ferritin- TIBC-
serum iron- LOW ferritin- LOW TIBC- HIGH Hb- LOW MCV- LOW transferrin- HIGH transferrin sat- LOW
46
how much iron in an adult?
3-5grams
47
what are the 3 pools that iron can be located in?
1) metabolic pool: Hb and myoglobin (2-3g) 2) storage pool: ferritin and haemosiderin (1g) 3) transit pool: plasma protein bound (transferrin bound) (3mg)
48
what is iron a positive regulator for? what is it a negative regulator for?
positive for erythropoiesis and ferritin genes negative for transferrin receptor gene (transferrin receptor located on red blood cells) i.e. iron is pro storage, doesn't want to be moving much
49
what is irons interaction with transferrin receptor?
the iron complexes with the receptor and is internalised into the erythroblast transferrin is recirculated once iron is removed from it
50
hypochromic microcytic anaemia
- less Hb (therefore low MCH) - lower concentration of Hb (hence hypochromic, low MCHC) - microcytic due to low MCV
51
what are the 3 commonest reasons for hypochromic microcytic anaemia?
1) iron deficiency 2) thalassemia 3) anaemia of chronic disease milder forms of thalassemia cause microcytosis without the anaemia
52
what is the major cause of iron deficiency ?
blood loss due to menstruation due to gastrointestinal
53
what are the other causes of iron def apart from bleeding?
- dietary deficiency low dietary intake in vegans and vegetarians - increased needs pubertal growth during child bearing - malabsorption (less common) menstruating women and growing children usually have poor diet as a cause of iron def
54
what oral iron compound is commonly used for iron replacement treatment?
ferrous sulphate (high iron content)
55
what are the side effects of ferrous sulphate?
- constipation - indigestion these reduce compliance therefore ferrous fumarate or ferrous gluconate with less iron may be better tolerated may need to be given parenterally
56
how does SERRUM FERRITIN help distinguish the different causes of anaemia
1) uncomplicated iron deficiencies --> LOW serum ferritin 2) thalassemia trait--> NORMAL serum ferritin 3) ACD--> RAISED or NORMAL serum ferritin As ferritin is an acute phase reactant, however, it may be normal or increased in patients where iron deficiency co-exists with chronic inflammatory conditions.
57
what is Anaemia of Chronic Disease associated with?
chronic inflammatory, infectious or neoplastic condition
58
what sort of anaemia does ACD usually cause?
mild-moderate normocytic/microcytic hypochromic anaemia
59
what are the inflammatory markers of ACD?
- C-reactive protein - ESR (erythrocyte sedimentation rate) both of these are raised
60
why does ACD causes hypochromia?
failed incorporation of iron into erythroblast causes reduced Hb synthesis
61
what are serum ferritin levels in those with ACD AND IDA?
low in the normal range
62
how can ACD and IDA be distinguished?
bone marrow aspirate

MCD Haematology (11 decks)

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