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Haemotology > Microcytic anaemia and Iron metabolism > Flashcards

Microcytic anaemia and Iron metabolism Flashcards

1
Q

microcytic anaemias

A
  • Reduced rate of haemoglobin synthesis
  • Erythrocytes smaller than normal (microcytic)
  • Cells often paler than normal (hypochromic)
    • Less haemoglobin
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2
Q

microcytic anaemias are due to

A

1) reduced haem synthesis
2) reduced glonbin chain synthesis

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3
Q

1) Reduced haem synthesis causes

A
  • Iron deficiency
    • Insufficient iron for haem synthesis
  • Lead poisoning (rare)
    • Acquire defect
    • Lead inhibits enzymes involved in haem synthesis
  • Anaemia of chronic disease
    • Hepcidin results in functional iron deficiency
  • Sideroblastic anaemia
    • Inherited defect in haem synthesis
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4
Q

2) Reduced globin chain synthesis causes

A
  • Alpha thalassaemia
    • Deletion or loss of function of one or more of the 4 alpha globin genes
  • Beta thalassaemia
    • Mutation in B globin genes leading to reduction or absence of the B globin
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5
Q

acronymn for microcytic anaemia

A

TAILS

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6
Q

T

A

thalassaemia

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7
Q

A

A

anaemia of chronic disease

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8
Q

I

A

iron deficiency

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9
Q

L

A

lead poisoning

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10
Q

S

A

sideroblastic anaemia

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11
Q

iron is an essential element in all livign cells. Required for

A
  • Oxygen carriers
    • Hb in red cells
    • Myoglobin in myocytes
  • Co-factor in many enzymes
    • Cytochrome (oxidative phos)
    • Kreb cycle enzymes
    • Cytochrome P450 enzymes (detoxification)
    • Catalase
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12
Q

free iron is

A

potnetially very toxic

  • Complex regulatory systems to ensure the safe absorption, transportation and utilisation
  • Body has no mechanism for excreting iron- important concept
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13
Q

iron can exist in a rnage of oxidation states- what are the most common

A

ferrous iron (Fe2+) and ferric iron (Fe3+

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14
Q

Fe2+

A

ferrous iron

  • reduced form
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15
Q

Fe3+

A

ferric iron

oxidised form

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16
Q

dietary iron consists of

A

haem iron (Fe2+) and non-haem iron (mixture of Fe2+ and Fe3+)

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17
Q

what must happen to ferric (Fe3+) iron before it can be absorbed from the diet

A

must be reduced to ferrous (Fe2+)

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18
Q
A
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19
Q

where does absorption of ferrous iron (Fe2+) occur

A

duodenum and upp jejunum

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20
Q

is haem or non-haemi iron best

A

haem iron (pure Fe2+)

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21
Q

good source of haem iron

A

liver, kidney, beef steak, chicken, duck, salmon/tuna

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22
Q

good soruce of non-haem iron

A

fortified cereals

rasiins

beans

figs

barley

oats

rice

potatoes

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23
Q

Dietary absorption of iron

A
  • In the upper duodenum region that absorption occurs
  • Haem iron (Fe2+ ferrous) can be absorbed without transporters
  • Non haem iron needs transporter
    • Fe3+ à Fe2+
    • Reductase uses vitamin C to reduce ferric to ferrous
    • Fe2+ can then be absorbed via DMT1 (divalent (meaning 2- fe2+) metal transporter 1) cotransporter
  • Haem is degraded within the enterocyte to release Fe2+ (haem oxygenase)
    • Iron can be stored as ferritin (Fe3+)
    • Iron can be transported into the blood via ferroportin
  • To transport iron around the body it is bound to a protein called Transferrin (binds 2 ferric Irons – Fe3+)
    • Hephaestin converts Fe2+ to Fe3+
  • Hepcidin inhibits the function of ferroportin
24
Q

factors affecting absorption of Non-haem iron from foods:

Negative influence

A

Tannins (tea)

  • Phytates (e.g. chapattis, pulses)
  • Fibres
  • Antacids (e.g. Gaviscon)
25
Q

factors affecting absorption of Non-haem iron from foods:

Positive influence

A
  • Vitamin C and citrate
  • Prevent formation of insoluble iron compound
  • Vit C also help reduce ferric to ferrous irons
    • E.g. take iron tablets with orange juice
26
Q

Functional iron (3350mg)

A
  • Haemoglobin (~2000 mg)
  • Myoglobin (~300 mg)
  • Enzymes e.g. cytochromes (~50 mg)
  • Transported iron (in serum mainly in transferrin) (~3 mg)
27
Q

Stored iron (around 1000 mg)x

A

Ferritin (soluble)

o Globular protein complex with hollow core

o Pores allow iron to enter and be release

Hemosiderin (insoluble)

o Aggregates of clumped ferritin particles, denatured protein and lipid

o Accumulates in macrophages, particularly in liver, spleen and marrow

28
Q

cellular uptake of iron from the blood

A
  1. Fe3+ bound transferrin binds transferrin receptor and enters the cytosol receptor-mediated endocytosis
  2. Fe3+ within endosome released by acidic microenvironment and reduced to Fe2+
  3. The Fe2+ transported to the cytosol via DMT1.
  4. Once in the cytosol, Fe2+ can be stored in ferritin, exported by ferroportin (FPN1), or taken up by mitochondria for use in cytochrome enzymes
29
Q

ferritin structure

A

iron storage mocluel with iron mineral core (found within cells)

30
Q

Iron recycling

A
  • Only small fraction of daily iron requirement gained from diet
  • Most (80%) of iron requirement met from recycling damaged or senescent red blood cells
31
Q

features of iron recyling

A
  • Old RBCs engulfed by macrophages via phagocytosis
  • Mainly splenic macrophages and Kupffer cells of liver
  • Macrophages catabolise haem released from RBC
  • Amino acids reused and iron exported to blood (transferrin) or returned to storage pool as ferritin in macrophage
32
Q

Regulation of iron absorption

A
  • Depends on dietary factors, body iron stores and erythropoiesis
  • Dietary iron levels sensed by enterocytes
  • Control mechanisms
    • Regulation of transporters e.g. ferropotin
    • Regulation of receptors e.g. transferrin receptor & HFE protein (interacts with transferrin receptor)
    • Hepcidin and cytokines
    • Crosstalk between the epithelial cells and other cells like macrophages
33
Q

hepcidin

A

a key negative regulator of iron absorption

34
Q

how does hepcidin work

A
  • During iron overload hepcidin synthesis is increased
    • Induced internalisation and degradation of ferroportin
35
Q

hepcidin synthesis is decreased by

A

high erytrhopoieric activity

36
Q

anaemia of chronic disease is what sort of iron deficiency

A

functional iron deficiency

37
Q

mechanism of anaemia of chronic disease

A
  1. Main mechanism: cytokine IL-6 released by immune cell due to inflammatory condition such as arthritis
  2. IL-6 increases the production of Hepcidin by liver
    • Inhibition of ferroprotein
    • Decreased iron released from retinoendothelial system
    • Decreased iron absorption in the gut
      • Plasma iron reduced
      • Inhibition of erythropoiesis in bone marrow
  3. IL-6 also inhibits erythropoietin, further inhibiting erythropoiesis
38
Q

summary of iron homeostasis

A
39
Q

Iron deficiency

A
  • Most common nutritional disorder worldwide
  • 1/3rd of world population are anaemic with at least half of these due to iron deficiency
40
Q

iron defiicnecy is a ….. not a ……

A

sign not a diagnosis

need to seek underlying reason why patient is iron deficiency

41
Q

causes of iron deficiency

A
  • Could be due to:
    • Insufficient intake/ poor absorption
      • Vegan and vegetarian diets
    • Physiological reasons e.g. pregnancy and rapid growth (increased requirement)
    • Pathological reasons e.g. bleeding
      • Menstruation
      • Gastric bleeding due to chronic NSAID usage
    • Anaemia of chronic disease e.g. IBD
42
Q

groups at risk of iron deficiency

A
  • Infants
  • Children
  • Women of child bearing age
  • Geriatric age group
43
Q

physiological effects of iron deficiency (same as anaemia)

A
  • Tiredness
  • Pallor
  • Reduced exercise tolerance (due to reduced oxygen carrying capacity)
  • Cardiac- angina, palpitations, development of heart failure)
  • Increased respiratory rate
  • Headache, dizziness, light-headedness
44
Q

other symptoms of iron deficiency

A
  • Pica – unusual cravings for non-nutritive substances e.g. dirt and ice
  • Cold hands and feet
  • Epithelial changes
45
Q

sings of iron deficiency

A

angular cheilitis

glossitis

koilonychia (spoon nails)

46
Q

Iron deficiency anaemia: FBC results

A
  • Low mean corpuscular volume (MCV)
  • Low mean corpuscular haemoglobin concentration (MCHC)
  • Often elevated platelet count (>450,000/μL)
  • Normal or elevated white blood cell count
  • Low serum ferritin, serum iron and %transferrin saturation, raised TIBC
  • Low Reticulocyte Haemoglobin Content (CHr)
47
Q

Peripheral blood smear results in iron deficiency anaemia

A
  • RBC are microcytic and hypochromic in chronic cases
  • Anisopoikilocytosis- change in size and shape
  • Sometimes pencil cells and target cells
48
Q

Testing for iron deficiency

A
  • Plasma ferritin commonly used as indirect marker of total iron status
    • Ferritin predominantly a cytosolic protein but small amounts are secreted into the blood where it functions as an iron carrier
  • Reduced plasma ferritin definitively indicates iron deficiency
  • BUT.. Normal or increased ferritin does not exclude iron deficiency
    • Ferrtitin levels can also increase considerably in cancer, infection, inflammation, liver disease and alcoholism
  • CHr (reticulocyte haemoglobin content) recommended by NICE to test for functional iron deficiency
  • CHr remains low during inflammatory responses etc. (also low in those with thalassaemia)
49
Q

Treatment of iron deficiency

*

A
  • Dietary advice
  • Oral iron supplements
    • Safest, first-line therapy for most patients but many experience GI side effects and compliance with treatment
  • Intramuscular iron injections
  • Intravenous iron
  • Blood transfusion- only used if severe anaemia with imminent cardiac compromise
50
Q

iron excess is

A

dangerous

  • Excess iron can exceed binding capacity to transferrin
  • Excess iron deposited in organs as haemosiderin
  • Iron promotes free radical formation and organ damage
    • E.g. plays a role in the Fenton reaction which creates free radicals
51
Q
A
52
Q

causes of iron excess

A
  • Transfusion associated hemosiderosis
  • Hereditary hemochromatosis (HH)
53
Q

Transfusion associated hemosiderosis is caused by

A
  • Repeated blood transfusions give gradual accumulation of iron
  • 400ml blood = 200mg iron
  • Problem with transfusion dependent anaemias such as thalassaemia & sickle cell anaemia
  • Iron chelating agents such as desferrioxamine can delay but do not stop inevitable effects of iron overload
54
Q

transfussion asscoaited hemosiderosis leads to

A

Accumulation of iron (hemosiderin) in the liver, heart and endocrine organs:

  • Liver cirrhosis
  • Diabetes mellitus
  • Hypogonadism
  • Cardiomyopathy
  • Arthropathy
  • Slate great colour skin
55
Q

Hereditary heamochromatosis

A

Autosomal recessive disease caused by mutation in HFE gene (on Chr 6)

56
Q

HFE protein and hereditary haemochromatosis

A
  • HFE protein normally interacts with transferrin receptor reducing its affinity for iron-bound transferrin
  • HFE also promotes hepcidin expression through activation of signalling pathways in liver
  • Mutated HFE therefore results in loss of negative influences on iron uptake and absorption
  • Too much iron enters cells and accumulates in end organs causing damage
57
Q

results of HH

A
  • Liver cirrhosis
  • Diabetes mellitus
  • Hypogonadism
  • Cardiomyopathy
  • Arthropathy
  • Increased skin pigmentation

Haemotology (12 decks)

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