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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
Q

what are the lab signs of ACD?

A

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
Q

what conditions are associated with ACD?

A

o Chronic infections – e.g. TB/HIV.
o Chronic inflammation.
o Malignancy.
o Misc. – e.g. cardiac failure.

27
Q

what is the main pathogenesis mechanism of ACD

A

cytokine release
TNF alpha and IL
interference with iron transport

28
Q

how do cytokines lead to ACD?

A
  • 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
Q

what is the major cause of iron def?

A

blood

bleeding e.g. menstrual or GI bleed

30
Q

what are the minor causes of iron def?

A
  • increase use of iron e.g. pregnancy/ growth
  • dietary def e.g. vegetarian
  • malabsorption e.g. coeliac disease
31
Q

when are full GI investigations carried out for iron def?

A
  • males
  • women over 40, post-menopausal
  • woman with scanty menstrual loss
32
Q

what makes up a full GI investigation ?

A

upper GI endoscopy (oesophagus, stomach, duodenum)
duodenal biopsy
colonoscopy

if nothing is found a small bowel meal is given

33
Q

when is no investigation done?

A
  • a menstruating women <40 with heavy periods
  • multiple pregnancies
  • no GI symptoms
34
Q

what also can be investigated to find the cause of iron def?

A

urinary blood loss (renal tract)
antibodies for coeliac disease
bleeding cancers (chronic, low grade)

35
Q

what are the lab parameters in blood tests that would be useful in investigation?

A
  • serum iron
  • total iron binding capacity
  • transferrin saturation
  • serum ferritin
  • haemosiderin in bone marrow using Prussian blue solution
  • MCV
36
Q

causes of low MCV [3]

A

iron def
thalassemia trait
ACD

37
Q

serum levels in the causes of low MCV

A

iron def has low serum Fe
ACD has low serum Fe
thala. trait has normal Fe

38
Q

ferritin levels in the causes of low MCV

A

iron def has low ferritin

ACD has high ferritin (due to interfered transportation, nothing is moved from ferritin)

39
Q

why is ferritin not reliable in telling whether someone has iron def?

A

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
Q

transferrin levels in the causes of low MCV

A
  • iron def has a transferrin increase (attempt to use)

- ACD has normal or low transferrin (little transport)

41
Q

transferrin saturations in causes of low MCV

A
  • 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
Q

further investigation to blood test

A 
	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
Q

thalassemia trait parameter results:
serum iron-
ferritin-
TIBC- (same as transferrin level)

A

serum iron- NORMAL
ferritin- NORMAL
TIBC- NORMAL

Hb- LOW
MCV- LOW
transferrin- NORMAL
transferrin sat- NORMAL

44
Q

classic ACD parameter results:
serum iron-
ferritin-
TIBC- (same as transferrin level)

A

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
Q

classic iron def parameter results:
serum iron-
ferritin-
TIBC-

A

serum iron- LOW
ferritin- LOW
TIBC- HIGH

Hb- LOW
MCV- LOW
transferrin- HIGH
transferrin sat- LOW

46
Q

how much iron in an adult?

47
Q

what are the 3 pools that iron can be located in?

A

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
Q

what is iron a positive regulator for?

what is it a negative regulator for?

A

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
Q

what is irons interaction with transferrin receptor?

A

the iron complexes with the receptor and is internalised into the erythroblast

transferrin is recirculated once iron is removed from it

50
Q

hypochromic microcytic anaemia

A
  • less Hb (therefore low MCH)
  • lower concentration of Hb (hence hypochromic, low MCHC)
  • microcytic due to low MCV
51
Q

what are the 3 commonest reasons for hypochromic microcytic anaemia?

A

1) iron deficiency
2) thalassemia
3) anaemia of chronic disease

milder forms of thalassemia cause microcytosis without the anaemia

52
Q

what is the major cause of iron deficiency ?

A

blood loss

due to menstruation
due to gastrointestinal

53
Q

what are the other causes of iron def apart from bleeding?

A
  • 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
Q

what oral iron compound is commonly used for iron replacement treatment?

A

ferrous sulphate (high iron content)

55
Q

what are the side effects of ferrous sulphate?

A
  • 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
Q

how does SERRUM FERRITIN help distinguish the different causes of anaemia

A

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
Q

what is Anaemia of Chronic Disease associated with?

A

chronic inflammatory, infectious or neoplastic condition

58
Q

what sort of anaemia does ACD usually cause?

A

mild-moderate normocytic/microcytic hypochromic anaemia

59
Q

what are the inflammatory markers of ACD?

A
  • C-reactive protein
  • ESR (erythrocyte sedimentation rate)

both of these are raised

60
Q

why does ACD causes hypochromia?

A

failed incorporation of iron into erythroblast causes reduced Hb synthesis

61
Q

what are serum ferritin levels in those with ACD AND IDA?

A

low in the normal range

62
Q

how can ACD and IDA be distinguished?

A

bone marrow aspirate

MCD Haematology (11 decks)

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