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Metabolism, Endocrinology And Haematology > Introduction To Anaemia > Flashcards

Introduction To Anaemia Flashcards

1
Q

Define anaemia

A

A haemoglobin concentration lower than the normal range

  • the normal range will vary with age , sex and ethnicity
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2
Q

What are symptoms of anaemia ?

A
  • shortness of breath
  • palpitations
  • headaches
  • claudication
  • angina
  • weakness and lethargy
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3
Q

What are signs of anaemia ?

A

Pallor

Tachycardia

Systolic flow murmur

The tachypnoea

Hypotension

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4
Q

Why. Might anaemia develop ( 3 general causes )

A

1) Increased removal of RBC by the reticuloendothelial system or excessive blood loss.
2) Production of the RBC in bone marrow is dysfunctional or reduced.
3) RBC are produced but are abnormally functioning.

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5
Q

Why might anaemia develop from reduced or dysfunctional erthyropoiesis?

A

1) In chronic kidney disease the kidney can stop making EPO , which means that red blood cell production decreases.
2) BONE MARROW NOT RESPONDING TO EPO: this can occur from chemotherapy , toxicity( eg ionising radiation , drugs). Or parvovirus infection.
3) If marrow is infiltrated by cancer cells or fibrous tissue ( myeolfibrosis) the number of normal haemopoietic cells decreases.

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6
Q

How can defects in haemoglobin synthesis result to anaemia?

A

1) A/B thalassaemia. Sickle cell disease.
2) defects in the haem synthetic pathway can lead to sideroblastic anaemia
3) Insufficient Iron diet can lead to not enough iron to make haem.
4) Anaemia of chronic disease.

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7
Q

What are the 4 ways haemolytic anaemia may develop from abnormal structure and mechanical damage ?

A

1) INHERITED - hereditary spherocytosis
2) Acquired damage
3) G6PDH deficiency
4) Pyruvate kinase deficiency

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8
Q

How can hereditary spherocytosis lead to haemolytic anaemia ?

A
  • mutations in genes coding for proteins involved in interactions between the plasma membrane and cytoskeleton ( eg spectrin , ankyrin , band 3 , protein 4.3)
  • this causes cells to become less flexible and more easily damaged when they move through capillary fenestrations. More likely to lyse.
  • they either lyse or are removed more quickly by the RES.
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9
Q

Give examples of how acquired damage can lead to mechanical damage of RBC which leads to haemolytic anaemia ?

A

1) RBC undergo stress as they pass through a defective heart valve.
2) RBC snagging on fibrin strands in small vessels where there has been an increased activation of clotting cascade.
3) heat damage from severe burns
4) osmotic damage from drowning in freshwater.

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10
Q

What are schistocytes?

A

Fragments resulting from mechanical damage which is a good indicator that there is some form of pathology present.

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11
Q

How can G6PDH defiecency lead to defects red cell metabolism which can lead to haemolytic anaemia ?

A

Glucose 6 phosphate dehydrogenase defiency means that less NADPH would be produced.

  • NADPH is required for the reduction of oxidised glutathione
  • with glutathione not being reduced into its active reduced form (GSH) , this makes RBC more prone to oxidative damage.
  • this can lead to haemoglobin in RBC forming cross links between eachother - forming Heinz bodies.
  • this makes them more prone to lysis or removal from the RES.
  • HAEMOLYTIC ANAEMIA.
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12
Q

How can pryruvate kinase deficiency as an examp”e of defect in cell metabolism , result in haemolytic anaemia ?

A

1) Pyruvate kinase is the final enzyme in glycosides.
2) rare genetic defect in this enzymes results in limited production of glucose from glycolysis.
3) Because RBC do not have mitochondria , they rely on glycolysis to produce ATP.
4) Thus , a defective glycolytic pathway causes red cells to rapidly become deficient in ATP and undergo haemolysis.

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13
Q

How can anaemia develop from excessive bleeding ?

A

1) Acure blood loss for example injury , surgery , childbirth , ruptured blood loss
2) Chronic NSAID usage ( aspirin , ibuprofen , naproxen) which can induce GI injury or bleeding.
3) Chronic bleeding : menstrual bleeding , repeated nose bleeds , haemorrhoids , blood lost in stool , intenstinal cancer , kidney or bladder tumours.

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14
Q

Why does splenomegaly often occur with haemolytic anaemias ?

A

Because the spleen is doing extra work by trying to remove the damaged red blood cells. Thus it undergoes hypertrophy.

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15
Q

How can myelofibrosis lead to a decrease in red blood cell production which lead to anaemia ?

A

1) myelofibrosis is a rare type of bone cancer which results in too much fibrous tissue which leads to scarring of the bone marrow. This happens because of proliferation of mutated hematopoietic stem cells which causes marrow fibrosis.
2) Fibrotic bone marrow means there is little space for haemopoiesis.
3) mutated hematopoietic cells from bone marrow then colonise they liver and spleen which leads to extramedullary haemopoiesis. Such patients show enlarged liver and spleen.

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16
Q

How can thalassaemia lead to anaemia ?

A
  • inherited disorder resulting from mutant A or bglobin genes.
    2) This causes an imbalance between the alpha / beta globin chains.
    3) this results in defective microcytic hypochromic red cells
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17
Q

What are the two features we consider to help us work out the cause of anaemia ?

A

1) the red blood cell size : macrocytic , microcytic, normocytic
2) the president or absence of recticulocytosis - which an indication on whether the marrow has responded normally.

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18
Q

If the marrow is working normally in anaemia what would we expect to happen to recticulocyte count?

A

An increase in reticulocytes

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19
Q

If there is an increase in reticulocytes , what does this indicate during anaemia ?

A

Bone marrow is functioning normally

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20
Q

If there is an increase in reticulocytes number , what do we then consider ?

A

Is there evidence of haemolysis

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21
Q

What are good indications of haemolysis?

A

Whether there is a high bilirubin which indicates that red blood cells are being broken down.

2) HIGH LDH ( lactate dehydrogenase)

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22
Q

If there is evidence of haemolysis , what could be the possible causes ?

A

Autoimmune cause

Enzyme defects

Membrane defects

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23
Q

If there is no evidence of haemolysis, but there is an increase in the reticulocytes what should we then look for ?

A

Evidence of blooding

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24
Q

If there isn’t an increase in reticulocytes count , what does this indicate ?

A

Problem in the bone marrow

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25
Q

What should we then do , once there is no increase in reticulocytes?

A

Consider the blood indicted such as whether they’re microcytic , macrocytic , normocytic

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26
Q

What are the causes of microcytic anaemia ?

A

Thalassaemia

Anaemia of chronic diseases

Iron deficiency

Lead poisoning

Sideroblastic anaemia

27
Q

What are the causes of macrocytic anaemia ?

A

1) vitamin b12 defiance
2) folate deficiency
3) myelodysplasia
4) liver disease
5) alcoholic toxicity

28
Q

What are the causes of normocytic RBC ?

A

Primary bone marrow failure * aplastic anaemia)

Secondary bone marrow failure ( HIV eg )

29
Q

What is macrocytic anaemia ?

A

Where the average red cell size is greater than normal ( MCV higher)

30
Q

What is megablastic anaemia ?

A
  1. An anaemia of macrocytic classification where the bone marrow produces unusually large red blood cells.
    2) this occurs because there is an interference with DNA synthesis during erthyropoiesis which causes a delay in the development of the nucleus. The nucleus and cytoplasm of the RBC do not mature at the same rate.
    3) this results in cell division being delayed and the erthryoblasts continue to grow to form megaloblasts which give rise to larger RBC.
31
Q

What are a few causes of megablastic anaemias ?

A

Vitamin B12/ folate deficiency

  • drugs that interfere with DNA synthesis such as anti cancer drugs

-

32
Q

What is macronormoblastic erthyropoiesis?

A

An anaemia which is a class of macrocytic anaemia , where the red blood cells are abnormally large.

1) unlike megaloblatsic anaemia where the nucleus and cytoplasm mature at different rates , in macronormoblastic the cytoplasm and nucleus mature at the same rate but erthyroblasts are just much larger than normal and give rise to large red cells.

33
Q

What are a few causes of macronormoblastic erthyropoiesis?

A

1) liver disease
2) alcohol toxicity

3)

34
Q

What is stress erthyropoiesis?

A
  • this often occurs after blood loss due to haemorrhage or recovery from haemolytic anaemia where the high levels of erthyropoietin leads to an expanded and accelerated erthyropoiesis.
35
Q

What is folate ?

A

It is one of the B vitamins - often known as vitamin B9.

  • it Is synthesised in bacteria and plants
36
Q

Where is folate present in ?

A

Vegetable food sources for example green leafy vegetables.

37
Q

What is the synthetic form of folate called ?

A

Folic acid

38
Q

Where is folate mainly absorbed from ?

A

Dudodenum and jeunum

39
Q

What is the function of folate ?

A

Synthesis or nueclotide bases required for DNA and RNA synthesis S

40
Q

Folate stores in the liver , can last how many months ?

A

3-4 months

41
Q

What can cause a folate deficiency?

A

1) POOR DIET ( lack of green leaf vegetables)
2) Increased requirements for folate during pregnancy , severe skin diseases eg psoriasis , exfoliated dermatitis , increased erthyropoiesis.
3) disease of the duodenum and jejunum ( coeliac diseases and Crohn’s disease)
4) alcoholism
5) urinary loss of folate in liver disease and heart failure
6) drugs which inhibit dihydrofolate reductase.

42
Q

What are symptoms of folate deficiency?

A
  • shortness of breath
  • palpitations
  • headaches
  • angina
  • weakeness , lethargy
  • confusion
  • reduces sense of taste
  • diarrhoea
  • numbness and tingling of the feet and hands
  • depression
  • muscle weakeness
43
Q

What must pregnant women take during pregnancy ?

A

400micrograms of folic acid owe day within the first 12 weeks of pregnancy to prevent neural tube defects ( spina bifida)

-

44
Q

What is another term for vitamin B12.?

A

Cyanocobalamin

45
Q

Is vitamin B12 water or lipid soluble ?

A

Water soluble vitamin

46
Q

What is the function of vitamin B12?

A
  • essential contractor for DNA synthesis.
    2) required for erythropoiesis.
    3) essential for normal functioning of CNS
47
Q

What produces vitamin B12 ?

A

Bacteria only !

48
Q

Where can you find vitamin B12 - in what food sources ?

A

1) meat
2) fish
3) milk
4) cheese
5) eggs
6) yeast extract

49
Q

What people are at particular risk of experiencing vitamin B12 deficiency ?

A

People on a vegan diet

  • they need to take B12 supplement daily of 10 micro grams a day .
50
Q

How is vitamin B12 absorbed into the blood ?

A

1) B12 released from food proteins in stomach where it binds to haptocorrin. ( this is produced in the salivary gland)
2) This haptocorrin-B12 complex travels into the small intestine , where it would then be digested by pancreatic proteases, releasing B12 which would then bind to INTRINSIC FACTOR.
3) the B12-intrinsic factor complex then binds to CUBAM receptor which mediated uptake of the complex by receptor mediated endocytosis into ENTEROCYTES ( columnar epithelial cells)
4) after lysosomal release in enterocytes , B12 exits the enterocytes into the blood stream via MDR1.
5) B12 then binds to transcobalamin in blood and transported around blood stream.

51
Q

Where is the majority of B12 stored ?

A

Liver

52
Q

How long can vitamin B12 store in the liver last us ?

A

3-6 years

53
Q

What are the causes of vitamin B12 deficiency?

A

1) dietary deficiency: VEGAN
2) lack of intrinsic factor which means that B12 cannot bind to it in the small intestine and enter the enterocytes via receptor cell mediated endocytosis.
3) diseases of the ilium ( Crohn’s disease )
4) lack of transcobalamin ( cannot be transported in the blood - this is congenital )
5) chemical inactivation of B12 with the frequent use of anaesthetic gas nitrous oxide.
6) parasitic infection

54
Q

What type of anaemia results from lack of intrinsic factor in the small intestine ?

A

Pernicious anaemia.

55
Q

What is pernicious anaemia ?

A

Decreased or absent intrinsic factor which causes progressive exhaustion of B12 reserves .

  • this launches an immune response where AB( antibody) can either block binding of B12 to intrinsic factor or AB prevents receptor mediated endocytosis.

EITHER WAY B12 CANNOT BE ABSORBED BY THE BODY.

56
Q

What are symptoms of B12 defiance ?

A
  • those related to anaemia
  • mouth ulcers
  • glossitis ( sore / shiny tongue )
  • diarrhoea
  • paraesthesia

Disturbed vision

  • irratibilty
57
Q

Why is vitamin B12 defiance really dangerous ?

A

1) vitamin B12 defiance is associated with focal demyelination
2) it can also result in a serious condition called Subacute combined degeneration of posterior and lateral columns of the spinal cord.( irreversible )

58
Q

What are symptoms of subacute combine degeneration of the cord ?

A

Gradual onset of weakness

Numbness and tingling in arms , legs and trunk

Changes in mental state

59
Q

Why do B12 and folate defiance cause a megaloblastic anaemia ?

A

1) both folate and B12 defiance ultimately lead to thymidine deficiency
2) in the absence of thymidine , uracil is incorporated into DNA instead.
3) this results in asynchronous maturation between nucleus and cytoplasm, so the nucleus does not fully mature and cytoplasm matures at a normal rate.

60
Q

What are megaloblastic features in a peripheral blood film?

A
  • year drop red blood cells
  • oval shape red blood cells
  • hypersegmented neutrophils ( 6 or more lobes )
  • macrocytic red blood cells

-

61
Q

How to treat vitamin B12 deficiency?

A

For pernicious anaemia you should give hydroxycobalamine INTRAMUSCULAR not oral , this is because there is no intrisic factor so if you give oral medication then it wouldn’t be absorbed by the body.

This must be given for life.

  • for other causes of vitaminB12 deficiency give oral B12.
62
Q

What to be aware of when you give intramuscular hydroxycobalamine to someone with pefcinious anaemia ?

A

Hypokalaemia at the beginning,. This is due to increased K+ requirement as erythropoeisis increases back to its normal rate.

63
Q

How to treat folate deficiency?

A

Folic acid

Metabolism, Endocrinology And Haematology (23 decks)

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