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METABOLISM 2 > Anaemia > Flashcards

Anaemia Flashcards

1
Q

What is the lifespan of RBCs?

A

120 days

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2
Q

What is anaemia?

A

A low haemoglobin level

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3
Q

What is a ‘normal’ haemoglobin level?

A

There isn’t such a thing, it depends upon many factors including age, sex and race

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4
Q

What are symptoms of anaemia?

A

Tiredness, fainting, shortness of breath, worsening angina and palpitations

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5
Q

What are signs of anaemia?

A

Conjunctival pallor, rapid heart rate, systolic flow murmur, cardiac failure and retinal haemorrhages

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6
Q

What are the three main causes of anaemia?

A

Decreased production of red blood cells, increased destruction (haemolytic) or acute blood loss

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7
Q

What may cause the reduced production of red blood cells?

A

iron-deficiency, vitamin B12 or folate deficiency, bone marrow infiltration (e.g. cancer), any chronic disease and infections

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8
Q

What may cause excess haemolysis?

A

Disorders of the red blood cell membrane, enzymes or haemoglobin as well as a result of autoimmune destruction.

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9
Q

Define ‘macrocytic anaemia’

A

Mean corpuscular volume (MCV) of the erythrocyte is greater than 96fl

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10
Q

Define ‘normocytic anaemia’

A

MCV of the erythrocytes is between 76-96fl

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11
Q

Define ‘microcytic anaemia’

A

MCV of the erythrocytes is less than 76fl

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12
Q

What are the common causes of microcytic anaemia?

A

Iron-deficiency (most common) or thalassaemia

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13
Q

What are the common causes of macrocytic anaemia?

A

Folate or vitamin B12 deficiency

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14
Q

What are the common causes of normocytic anaemia?

A

Increase in haemolysis, increased blood loss cancer (bone marrow infiltration affecting erythropoiesis) or chronic disease

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15
Q

What is the treatment for iron-deficiency anaemia?

A

Replace the iron, either with dietary sources or supplementation (ferrous sulphate)

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16
Q

In what form must iron be in for it to be absorbed?

A

Fe2+ (not 3+) or bound to protein such as within haem.

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17
Q

Where is the majority of iron absorbed?

A

Enterocytes in the duodenum (these cells have iron transporter proteins)

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18
Q

How is free Fe3+ iron converted into the absorbable Fe2+ molecule?

A

Via the action of ferric reducatase on the brush border of enterocytes (predominantly in the duodenum)

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19
Q

What are transferrins?

A

These are glycoproteins found in the blood plasma that bind to iron to control the levels of free iron in the plasma and other extracellular fluids

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20
Q

How many molecules of free iron (Fe2+) can each transferrin molecule bind to?

A

2

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21
Q

How do transferrins deliver iron to tissues?

A

When bound to iron, the transferrin molecule will bind to a target cell that requires iron via a transferrin receptor on the surface. This causes the endocytosis of the complex and the acidic conditions cause the release of the free iron from the complex, and the transferrin complex is removed via exocytosis.

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22
Q

What is ferritin?

A

This is a large globular protein that stores iron and is food in most tissues in the cell cytosol, but can also function as an iron carrier in the serum.

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23
Q

What can plasma ferritin levels tell us?

A

Ferritin is a store of iron, and therefore, if there are low levels of ferritin, this means that there isn’t a lot of iron storage occurring, and therefore it can be indirectly inferred that there is a deficiency of iron due to poor residual stores

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24
Q

How do plant and animal sources of iron differ?

A

Plant iron is non-haem and absorption is often limited due to low solubility due to presence of powerful chelators (prevent iron dissociation), whereas red meat supplies haem iron which has a high bioavailability and is readily absorbed

25
Q

What factors aid in iron absorption?

A

Iron being in the haem form (from meat), being in Fe2+ form so it can be absorbed without conversion, acidic pH as this aids iron release from transferrin, pregnancy, hypoxia and iron-deficiency

26
Q

What factors impair iron absorption?

A

Iron being in the non-haem form (from vegetables), Fe3+ instead of Fe2+ presence, alkaline tissues (can be caused by PPI use for reflux), iron overload and inflammatory disorders

27
Q

What is anaemia of chronic disease?

A

A normocytic anaemia that occurs due to chronic inflammation, infection or cancer which can diminish the lifespan of RBCs, decrease erythropoiesis, reduce bone marrow responsiveness to EPO or reduce EPO production in the kidney

28
Q

Where is EPO produced?

A

Kidney

29
Q

What complication may haemolytic anaemia cause?

A

In chronic haemolytic anaemia, there is a large accumulation of bilirubin (as a result of erythrocyte breakdown) and this can lead to the formation of gallstones.

30
Q

What is the main cause of haemolytic anaemia?

A

Generally, it is caused by abnormalities of the individual’s red blood cells

31
Q

What membrane abnormalities may lead to haemolytic anaemia?

A

Hereditary spherocytosis, membrane damage from free radicals, autoimmune attack of the membrane (e.g. transfusion rejection)

32
Q

What haemoglobin abnormalities may lead to haemolytic anaemia?

A

Abnormal haemoglobin structure (sickle cell disease) or imbalance of alpha to beta chain synthesis, as in thalassaemia

33
Q

What intracellular enzyme abnormality may lead to haemolytic anaemia?

A

If there is glucose-6-phosphate dehydrogenase deficiency

34
Q

What is extravascular haemolysis?

A

Breakdown of the red blood cells occurs outside of the blood vessels, and this is physiological but can be caused by: sickle cell disease, thalassaemia, antibody-induced haemolytic anaemia, rhesus mismatched transfusion and hereditary spherocytosis

35
Q

What is intravascular haemolysis?

A

the breakdown of red blood cells occurs within the blood vessels and this is often caused b: ABO mismatched transfusion, snake bites and infections

36
Q

What is hereditary spherocytosis?

A

Autosomal dominant condition where there is a defect in RBC cytoskeleton which leads to the production of RBCs which have a spherical shape rather than bi-concave. This shape is functional but is more prone to physical degradation when passing through the splenic capillaries.

37
Q

How may glucose-6-phosphate dehydrogenase deficiency in erythrocytes lead to haemolytic anaemia?

A

Works to prevent and reverse haemoglobin oxidation (as a result of high oxygen exposure), therefore, without it the cells degrade far more quickly. This occurs due to an X-linked condition.

38
Q

What is autoimmune haemolytic anaemia?

A

When IgG antibodies in the blood detect the antigens on the RBCs as foreign and bind and take them to the spleen to be haemolyses.

39
Q

What is the clinical presentation for haemolytic anaemia?

A

Generic symptoms of anaemia such as pallor, as well as clear jaundice, potential for gallstones and splenomegaly also.

40
Q

How does haemolytic anaemia appear in lab tests?

A

Increased serum bilirubin and lactate dehydrogenase levels. In a blood film, there is a compensatory increase in erythropoiesis so there will be more reticulocytes and increased RBCs in the bone marrow.

41
Q

How does vitamin B12 or folate deficiency lead to macrocytic anaemia?

A

These molecules are required for DNA synthesis (converting homocysteine to methionine), so without these molecules, cells fail to divide and in erythropoiesis this leads to overlarge red blood cells.

42
Q

What is vitamin B12?

A

Vitamin B12 is a water-soluble vitamin that is found in meat and eggs, and it is not destroyed when these foods are cooked.

43
Q

How is vitamin B12 absorbed?

A

Vitamin B12 is usually bound to proteins in foods and is released as a result of stomach acid. Thereafter, the release vitamin B12 travels to the small intestine, and is largely absorbed in the ileum after binding to a protein known as intrinsic factor (IF).

Intrinsic factor is produced by the parietal cells of the gastric mucosae and it is then the IF-B12 complex that is then absorbed by receptors on the enterocytes in the ileum.

44
Q

What are the causes of vitamin B12 deficiency?

A

Restricted diet (veganism) leading to lack of intake, malabsorption due to IBS, disorder decreasing stomach acid production or gastric disorder so IF isn’t produced (pernicious anaemia)

45
Q

What is pernicious anaemia?

A

An autoimmune disorder that causes macrocytic anaemia that is characterised by vitamin B12 deficiency that is usually caused by the absence of intrinsic factor (this causes a deficiency as the B12 cannot be carried to the ileum and be absorbed).

46
Q

What causes pernicious anaemia?

A

It’s an auto-immune disorder whereby there is an autoantibody response against the gastric mucosa and intrinsic factor, and this also leads to gastric atrophy (due to autoimmune attack), decreased acid secretion and decreased intrinsic factor secretion.

47
Q

What are the risk factors for developing pernicious anaemia?

A

The condition is more prevalent in females than males and is often associated with fair hair, blue eyes and blood group A.

48
Q

What are the complications of pernicious anaemia?

A

This type of anaemia is fatal if left untreated as a vitamin B12 deficiency can cause irreversible neurological damage such as peripheral neuropathy, damage to sensory and motor tracts, dementia and optic atrophy.

49
Q

What is the clinical presentation of pernicious anaemia?

A

May illustrate mild jaundice due to accumulation of bilirubin from the excess breakdown of red blood cells as well as inflammation of the tongue, but mainly, neurological symptoms may be present due to the role of vitamin B12 in brain activity.

50
Q

What is the treatment for pernicious anaemia?

A

Treated with intramuscular vitamin B12 injections every three months for the rest of the individual’s life

51
Q

What is folate?

A

Folate is a water-soluble vitamin that is found in meat, vegetables, grains and nuts, but this vitamin IS destroyed by cooking (unlike B12).

52
Q

What are the common causes of folate deficiency?

A

IBS (especially of duodenum and jejunum), pregnancy, lactation and haemolytic anaemias (increase folate utilisation) or reduced dietary intake

53
Q

How can you identify vitamin B12 or folate deficiency from a blood film?

A

Red blood cells will appear larger, hypochromic and neutrophils will be hyper-segmented (~7 nuclear lobes)

54
Q

How can you identify vitamin B12 or folate deficiency from a blood count?

A

Decreased haemoglobin level, indication of macrocytic erythrocytes (MCV >96fl) and a reduction in the numbers of white blood cells and platelets

55
Q

How can you identify vitamin B12 or folate deficiency from biochemistry tests?

A

Lactate dehydrogenase (LDH) and bilirubin levels will be increased

56
Q

How may an individual with vitamin B12 or folate deficiency present?

A

The condition has a gradual onset (insidious), they may have conjunctival pallor, they may have a large and inflamed tongue (glossitis), mild jaundice, and neurological signs (only in B12 deficiency).

57
Q

Where is vitamin B12 mainly absorbed?

A

Ileum

58
Q

Where is folate mainly absorbed?

A

Duodenum and jejunum

METABOLISM 2 (33 decks)

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