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Haematology Sem 1 > 2. Anaemia > Flashcards

2. Anaemia Flashcards

1
Q

What are the components of haemoglobin?

A

Haem and globin. They are both haemoproteins.

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2
Q

Describe the structure of haemoglobin

A

Tetramer with 4 polypeptide pairs. There are two pairs of unlike polypeptide chains : 2 alpha pairs and 2 beta pairs.

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3
Q

Where is the haems contained?

A

In a hydropbic compartments of the globins

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4
Q

How many irons can fit on each haemoglobin?

A

4 Fe 2+

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5
Q

What is the redox reaction?

A

Fe 2+ to Fe3+ (ferrous state to ferrate)

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6
Q

In what oxidation state is iron when in circulation?

A

Fe2+

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7
Q

Why is iron Fe2+ when in circulation?

A

in order to maintain osmotic equilibrium

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8
Q

How to blood cells generate ATP?

A

Through the embden-meyerhof pathway

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9
Q

How do red cells generate power?

A

Through NADPH though hexose-monophosphate pathway

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10
Q

How is iron transferred around the body?

A

1) Iron binds to transferrin to form an iron-transferrin complex
2) Iron-transferrin complex transported to cells with transferrin receptors

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11
Q

What is ferritin?

A

Stored iron

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12
Q

Besides ferritin, what else can iron be stored as?

A

Haemosiderin

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13
Q

Where is ferritin stored?

A

Spleen, liver, pancreas and bone marrow

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14
Q

How many Fe mg does the western diet have?

A

10-15 mg-

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15
Q

Where is the iron absorbed?

A

5 - 10% through small intestine

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16
Q

Humans lose 1mg of iron a day. How?

A

through faeces, hair, skin, menstruation

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17
Q

Where can iron be found in the diet?

A

Red meat - liver in particular (animal iron is more readily absorbed than plant-based iron)
Egg yolk
Fish - sardines, tuna, salmon
Cereals, Wholemeal bread
pluses, legumes, veg, nuts, prunes and fortified foods

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18
Q

What is the meaning of anaemia?

A

To have below normal levels of haemoglobin

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19
Q

What are the normal ranges of haemoglobin for males and females?

A

male 130-170g/L. Female 120-155g/L

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20
Q

How is anaemia classified?

A

By the size of the red blood cells

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21
Q

What is microcytic anaemia? Mean cell volume?

A

Small red cells. MCV= <78fl/L

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22
Q

What is macrocytic anaemia? Mean cell volume?

A

Large red cells. MCV= >100fl/L

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23
Q

What is normocytic anaemia? Mean cell volume?

A

Normal red cell. MCV = 77-100fl/L

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24
Q

What kind of anaemia do microcytic cells cause?

A

Iron deficiency anaemia, thalassaemia, anaemia of chronic disease (and other haemoglobin disorders)

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25
Q

What are the two subcategories of macrocytic anaemia?

A

Megaloblastic anaemias and non-megaloblastic anaemias

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26
Q

What disorders/deficiencies may cause macrocytic megaloblastic anaemia?

A

B12 deficiency, Folic acid deficiency, and auto-immune disease (pernicious anaemia)

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27
Q

What is pernicious anaemia

A

anaemia caused by the auto-immune system

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28
Q

What disorders may cause macrocytic non-megaloblastic anaemia?

A

Liver disease, myeloidysplastic syndrome (MDS)

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29
Q

What kind of anaemias are caused by normoblastic cells?

A

Haemolytic, anaemia of chronic disease

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30
Q

If a patient suffers with acute blood loss, which kind of anaemia are they likely to have?

A

normocytic anaemia

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31
Q

What is the most common type of anaemia?

A

Iron deficiency anaemia

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32
Q

What are the two main causes of iron deficient anaemia?

A

Iron supply does not meet demand due to: Mean cell volume reduced, mean cell haemoglobin reduced.

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33
Q

What do microcytic anaemia red cells look like?

A

Central area of pallor is pale and empty. Small red cells.

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34
Q

What are the three main stages of iron deficient anaemia?

A

Iron repletes, iron depletes, iron deficient

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35
Q

What are the physical causes of iron deficient anaemia?

A

chronic blood loss due to menstrual cycles, gastrointestinal issues.
Increased demands due to growth or pregnancy
Malabsoption form stomach (due to gastrectomy)
Poor diet

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36
Q

How quickly do the clinical features of iron-deficient anaemia arise?

A

slowly

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37
Q

What are the clinical features of iron-deficient anaemia

A

pallor, fatigue, brittle hair and nails, dysphagia (issues swallowing) glossitis (tounge swelling), abnormal appetite, lassitude (lethargy) and trachychardia

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38
Q

What are the laboratory findings when studying a blood sample of an iron-deficient anaemia patient

A

hyperchromic (pale red cells)
microcytic cells
raised platelet count
Bone marrow will show absence of ferritin
Erythroblasts will be ragged/have an irregular cytoplasm
There is a reduced serum ferritin level and low serum iron levels
Raised serum transferrin receptors present (due to no transferrin binding to it)

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39
Q

What is the treatment for iron deficient anaemia?

A

Oral iron tablet taken 3x a day for 4-6 months.

IV iron for patients with malabsorption (which is the true cause of the illness)

40
Q

What response would you expect to see after treating iron-deficient anaemia?

A

You would expect a an increase in reticuloctye formation and circulation after 7 days of treatment

41
Q

What is the function of B12?

A

Coenzyme for 2 biochemical reactions:

1) methylation from homocystein to methionine
2) converts methylmalomyl coA to succinyl co A

42
Q

What would happen is the coenzyme reactions of B12 could not occur?

A

Less precursors for DNA synthesis and myelin production (for myelin sheath)

43
Q

What is the effect of abnormal DNA synthesis on RBC production?

A

Erythroblasts in bone marrow show abnormal maturation (maturation arrest - they are premature)
The maturation of the nucleus of the cell is delayed in relation to the cytoplasm
No reticuloctye production

44
Q

How many mg of B12 do adults require per day?

A

1ug

45
Q

How many mg of B12 would you expect in the normal, balanced diet?

A

10-15ug

46
Q

How long is B12 stored for?

A

2-4 years

47
Q

Where is B12 stored in the body?

A

In the liver

48
Q

Describe the process of absorption of B12 by the body

A

B12 absorbed in the illium of the small intestine by binding to intrinsic factors that have been secreted by the stomach. (ileum has receptors for these intrinsic factors so B12 absorbed when attatched)

49
Q

How is B12 transported through the body?

A

Travels through blood plasma when bound to transcobalamin

50
Q

How is B12 lost from the body?

A

Faeces and bile excretions

51
Q

What are the dietry sources of B12?

A 
Animal based produce:
liver, kidney, heart, red meat
clams, oysters, seafood,
Egg, cheese, milk, yoghurt,
fortified foods
52
Q

What are the main causes of B12 deficiency? (6)

A

Inadequate diet: vegans
Malabsoption: 1) due to gastrectomy (removal of stomach). 2) intrinsic factor deficiency so no absorption in ileum
Intestinal issues: Crohn’s, tape worm, ileal resection (due to crohns)
Excess utilisation of B12: 1)pregnancy 2)haematological disorder
Liver disease
Drug treatment

53
Q

What type of anaemia are you likely to experience with a B12 deficiency?

A

Megaloblastic anaemia

54
Q

What is megaloblastic anaemia

A

Type of macrocytic anaemia where DNA does not pass the G2 phase so continuously divides (leading to macrocytosis)

55
Q

What are the clinical features of megaloblastic anaemia (B12 deficiency)

A 
Slow onset
Mild jaundice
Glossitis
Tingling of hands and feet
Reduced platelet count
Raised biliruben levels
Low serum B12
Hypercellular bone marrow (maturation arrest)
Raised serum methiomalonic acid and homocytein levels
56
Q

Treatments of B12 deficiency?

A

1mg of hydroxycobalamin injected intramuscularly everyday 3 days until 6 injections have been given in total. Thereon after its just 1 every 3 months unless cause of B12 deficiency is resolved.

57
Q

What can be given alongside B12 treatment? Why?

A

K+ given at same time as B12 in severe cases as some people will die suddenly due to sudden drop in K+

58
Q

What is B12 neuropathy?

A

subacute degernation of the cord: progressive damage to peripheral sensory nerves (spinal cord, brain, peripheral nerves)

59
Q

Describe what the clinical features of B12 neuropathy would be

A

Clinical features mainly affect lower limbs. Tingling feet, difficulty walking (abnormal gait), falling often, optic atrophy, psychiatric conditions

60
Q

What is the cause of B12 neuropathy

A

Accumulation of homocystein and reduction in methionine in nervous tissues
This causes defective myelination of myelin
Abnormal fatty acids form around cell and nerves

61
Q

What is pernicious anaemia?

A

It is an autoimmune disease where auto antibodies attack gastric parietal cells. Parietal cells secrete intrinsic factors that bind to B12 and are later absorbed by the ileum. If parietal cells are attacked there will be no resorption of B12.

62
Q

What is the prevalence of pernicious anaemia?

A

Affects more women than men (1.6:1). Patients tend to be over the age of 60 and although common to all races, most common to northen europeans

63
Q

What secondary disease can result from pernicious anaemia?

A

Carcinoma of the stomach

64
Q

What is folic acid the parent group of?

A

the folates

65
Q

What does pteroglutamic acid refer to?

A

Folic acid

66
Q

What vitamin is folic acid?

A

B9

67
Q

How long is folic acid stored for?

A

3 months

68
Q

Can humans synthesise folic acid?

A

No

69
Q

When preparing food that is rich in folic acid, what must you not do to it?

A

Cook it: folic acid is heat sensitive and is destroyed by cooking

70
Q

Where is folic acid absorbed?

A

Jejunum

71
Q

What causes folic acid deficiency

A

malfunction of the small intestine: coeliacs disease, crohns disorder, tropical sprue

72
Q

What is the role of folic acid?

A

Required for metabolic reactions: homocystein to methionene, serine to glycine, DNA precursor synthesis
Necessary for the production of new cells
Substrates are important for reactions that involve B12 (homocystine to methionene and methylolmalomyl coA to Succinyl Co A)

73
Q

What does folic acid deficiency hinder?

A

Cell division and DNA synthesis

74
Q

What are the sources of folic acid?

A

Leafy veg (spinach), turnip, lettuce, liver, beans, peas, breakfast cereals, bananas, melon, lemons

75
Q

What are the cinical features of folic acid deficiency?

A

Same as B12 but less severe but does not cause neuropathy

76
Q

How quickly do symptoms appear?

A

Quickly as there arent as many reserves

77
Q

What causes folic acid deficiency?

A

Usually dietry - alcoholism or intestinal disorders

78
Q

When can demand for folic acid increase?

A

Pregnancy and during rapid cell division (cancer)

79
Q

What kind of disorder is spina bifada?

A

neural tube defect

80
Q

What cuases spinal bifada?

A

B12 or folic acid deficiency in early pregnancy. The lower the serum B12 or folate, the greater the incidence.
Homocystein builds up in the featus and impairs myelination of protiens and lipids

81
Q

What is the treatment for spina bifada?

A

No treatment just dietry supplements in early pregnancy

82
Q

What other abnormalities can arise from B12/folic acid deficiency?

A
  • sterility of either sex
  • abnormal morphology of cervix, bladder and other epithelia
  • cleft lip/pallate in feotus/newborn (folic acid supplements at conception/early pregnancy)
  • melanine pigmentation problems
  • CV and malignent disease
83
Q

What is normocytic anaemia?

A

Normal sized red cells but just not enough of them

84
Q

What causes normocytic anaemia?

A

Acute blood loss and premature destruction of red cells

85
Q

What would cause the premature distruction of red cells?

A

Haemolytic anaemia or chronic disease

86
Q

What are 3 diseases associated with haemolytic anaemia?

A

sickle cell, autoimmune disorders and hereditary spherocytosis

87
Q

What 4 kinds of heritary disease can cause haemolytic anaemia?

A

rheumatoid athritis, cancer, kindey disease or drug treatment

88
Q

What is haemolytic anaemia?

A

increased rate of RBC breakdown

89
Q

What are the two subcatercategories of haemolytic anaemia?

A

Hereditary or aquired

90
Q

What causes hereditary haemolytic anaemia? (3)

A

1) Red cell membrane defects: sperocytosis which causes RBC to be shperical as opposed to biconcave. Ellipotosis where RBC are elliptical shape.
2) Defective red cell metabolism: G6PD deficiency. Pyruvate kinase deficiency.
3) Disorders of haemoglobin synthesis: sickle cell, thallasaemia

91
Q

What are the two subcategories of acquired haemolytic anaemia?

A

Extra corpuscular and environmental

92
Q

What causes extracorpuscular haemolytic anaemia?

A

haemolytic disease of a newborn, autoimmune haemoltic anaemia, DIC and heart valve replacement

93
Q

What casues environental haemolytic anaemia?

A

Drug induced, march haemoglocinuria and infetion of malaria, ecoli

94
Q

What are the clinical effects of haemolyic anaemia?

A

Pallor, mild fluctating jaundice

95
Q

What would lab findings show if looking at haemolytic anaemia blood?

A

increased RBC breakdown: biliruben will be raised, hepatoglobin reduced. (hepatoglobin is binded to released haem and taken to spleen)
increased RBC production: increased reticulocytosis, bone marrow erthythrocyte hyperplasia (bone marrow enlarged due to extra production of RBC produced in its marrow)
Damaged red cells: morphology shows fragments, microspocytes and elliptocytes.

Haematology Sem 1 (8 decks)

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