IDA And ACD Flashcards

1
Q

Describe how the RBC carries out its functions

A
  • CO2 removal occurs by the RBC taking up CO2 and together with carbonic anhydrase forming H+ and bicarbonate (using Hb as a buffer). Bicarbonate is then exchanged for Cl- (chloride shift)
  • oxygen delivery can occur because Hb can bind reversibly to O2 without undergoing oxidation or reduction
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2
Q

Describe the RBCs functional shape

A

Shaped as a biconcave disc
- for maximal deformability (able to bend and fit through small blood capillaries)
- to increase surface area (for maximal gas transfer

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3
Q

What is the role of transferrin and its features?

A
  • transferrin is what iron binds to for transport in the plasma (responsible for iron delivery to all tissues, erythroblasts, hepatocytes and muscle)
  • it is a glycoprotein synthesised in hepatocytes (dependent on amount of iron stores in the body)
  • has 2 iron binding domains
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4
Q

What is the role of hepcidin?

A

Controls the amount of iron absorbed in duodenum and released from macrophages in the RES system.

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5
Q

How is iron taken up in erythroblasts?

A
  • erythroblasts have transferrin receptor on its surface which allows iron bound transferrin to be rapidly taken into cell
  • either taken to mitochondrion to be converted to haem or stored as ferritin (insoluble)
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6
Q

How is iron taken up by macrophages?

A
  • iron is taken up by macrophages by phagocytosing RBCs which are reaching the end of their life cycle
  • haem from RBC is broken into amino acids, in-conjugated bilirubin and iron
  • iron is stored in macrophages as ferritin or release to transferrin in the plasma
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7
Q

Describe how hepcidin regulates iron metabolism

A
  • hepcidin (‘low iron’ enzyme) binds to ferroportin causing degradation preventing iron absorption and release from RES
  • requires expression of HFE gene
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8
Q

What is the clinical relevance of hepcidin?

A

In hereditary haemochromatosis there is a mutation to the HFE gene resulting in the loss of hepcidin which is what causes iron overload

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9
Q

Describe the appearance of the cells in IDA

A
  • pale hypochromic and microcytic cells
  • cells cannot produce haem
  • <15% saturation of iron
  • reduced serum ferritin and Hb
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10
Q

What are other causes of hypochromic microcytic RBCs that are not IDA?

A
  • thalassaemia (not enough globin)
  • anaemia of chronic disease (can be normocytic and normochromic too)
  • sideroblastic anaemia
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11
Q

What is a problem associated with serum ferritin?

A

It is also an acute phase protein which poses a risk of IDA in times of tissue inflammation

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12
Q

What are the clinical signs of IDA?

A
  • koilonychia
  • atrophic glossitis (smooth tongue)
  • angular stomatitis
  • oesophageal web (Plummer syndrome - web-like membranes in throat causing dysphagia and problems swallowing)
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13
Q

What is the golden rule for patients presenting with IDA?

A
  • IDA in males and post-menopausal females is due to GI blood loss until proven otherwise
  • in young women assume to be menstrual/pregnancy related. GI investigations only if in presence of GI symptoms or blood in stools
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14
Q

What is the treatment for IDA?

A
  • iron replacement (if GI upset caused, reduce amount of elemental iron in makeup)
  • IV iron replacement (if intolerant, for complaince, for renal anaemia/epo replacement)
  • discover and resolve cause
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15
Q

What happens to iron in anaemia of chronic disease?

A
  • failure of utilisation of iron = reduced epo response or insensitivity
  • iron trapped in macrophages of RES (raised levels of hepcidin)
  • depressed marrow activity (depression caused by cytokines in inflammation, infection, or neoplasia)
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16
Q

What is the treatment for anaemia of chronic disease?

A

Treatment of the underlying cause

17
Q

What are the blood results expected in IDA/ACD?

A
  • MCV/MCH: normocytic normochromic/hypochromic microcytic
  • raised ESR
  • ferritin normal/raised
  • iron low
  • transferrin low