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Anaemia Flashcards

1
Q

How does a reduction in plasma volume effect Hb levels + when is this situation seen

A

Increases them

Dehydration

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2
Q

What are the three types of anaemias

A
  1. Hypochromic (low MCV)
  2. Normochromic (normal MCV)
  3. Microcytic (high MCV)
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3
Q

Why may some patients be asymptomatic for anaemia

A
  1. Slowly falling level of Hb = compensation as oxygen-dissociation curve will shift to the right, so that oxygen is more easily dissociated from Hb
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4
Q

Symptoms of anaemia

A
  1. Fatigue, headaches, faintness
  2. Breathlessness
  3. Angina
  4. Intermittent claudication
  5. Palpitations
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5
Q

How does anaemia additionally effect older people

A

Exacerbates cardiorespiratory problems

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6
Q

Clinical signs of anaemia

A
  1. Pallor
  2. tachycardia
  3. Systolic flow murmur
  4. Cardiac failure

SPECFIC:

  1. Koilonychia (spoon-shaped nails in longstanding iron deficiency anaemia)
  2. jaundice (haemolytic anaemia)
  3. Leg ulcers (associated with sickle cell)
  4. Bone deformities (thalassaemia)
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7
Q

Investigations for anaemia in peripheral blood

A

1, Red cell indices

  1. the WCC
  2. Platelet count
  3. Reticulocyte count (indictes marrow activity)
  4. Blood film
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8
Q

What should be seen on a blood film for anaemia

A

Two populations of red cells are seen - dimorphic

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9
Q

How is bone marrow investigated in anaemia

A
  1. Cellularity of marrow
  2. Type of erythropoiesis
  3. Infiltration of marrow
  4. Iron Stores
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10
Q

RBC lifespan

A

120 days

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11
Q

How does reticulocyte count correlate with bone marrow production measurement

A

Low count - Production of Bone marrow is an issue

High count - removal of bone marrow is an issue

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12
Q

What is MCV

A

Average volume of RBCs

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13
Q

What is the main cause of anaemia

A

Iron deficiency
Anaemia caused by chronic disease
Thalassaemia

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14
Q

What is the average intake of iron

A

15-20mg

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15
Q

How much of ingested iron is absorbed by the duodenum

A

10%

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16
Q

How is Iron absorbed

A
  1. AT into duodenal epithelial cells via HCP1 and incorporated into Ferritin
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17
Q

What happens to absorbed iron so it can travel in th blood

A

Bound to transferrin -> bone marrow to be incorporated into new erythrocytes

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18
Q

Where is iron stored in th body

A

Reticuloendothelial cells as FERRITIN or HAEMOSIDERIN (macrophages in bone marrow, liver and spleen)

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19
Q

Causes of iron deficiency anaemia

A
  1. Menorrhagia
  2. GI bleeding
  3. Hookworm (leading cause - GI blood loss)
    Poor diet
    Malabsorption
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20
Q

What happens to RBCs in iron-deficiency anaemia

A
  1. Crucial for haemoglobin production + reduction in iron = decrease in haemoglobin + smaller RBCs

MICROCYTIC ANAEMIA

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21
Q

Clinical presentation of iron-deficiency anaemia

A
  1. Brittle nails + hairs
  2. Koilonychia
  3. Atrophy of the tongue papilla
  4. Cheilosis (ulceration of mouth corners)
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22
Q

What are three differential diagnostics for iron-deficiency anaemia

A
  1. Thalassaemia
  2. Sideroblastic anaemia
  3. Anaemia of chronic disease
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23
Q

How is iron-deficiency anaemia diagnosed in blood tests

A
  1. RBCs and microcytic and HYPOCHROMIC (pale)
  2. Poikilocytosis (variation in shape) and anisocytosis (variation in size)
  3. Serum iron is low
  4. TIBC (total iron-binding capacity) rises to normal (transferrin below 19% saturation = iron deficiency)
    5
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24
Q

How does serum ferritin help in diagnosis

A

Level reflects amount of iron stored - confirms DIAGONSIS

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25
Q

What happens to the number of transferrin receptors in iron-defiiceny anaemia

A

Increases

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26
Q

Reticulocyte in iron deficiency anaemia

A

Low

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27
Q

How is Iron deficiency anaemia treated

A
  1. Oral Iron (FERROUS SULPHATE)
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28
Q

Side effect of ferrous sulphate

A

Nausea
Abdominal Discomfort
Diarrhoea/constipation
Black stools

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29
Q

What can be given as a replacement to serous sulphate if side effects are bad

A

Ferrous GLUCONATE

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30
Q

In extreme cases (e.g. severe iron malabsorption) what can be given

A

Parenteral iron

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31
Q

What is anaemia of chronic disease

A

Anaemia that is secondary to chronic disease = anaemia

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32
Q

RBC appearance in chronic disease anaemia

A

NORMOCYTIC (could be microcytic)

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33
Q

When can RBCs be microcytic in CDA

A

Rheumatoid and crohn’s disease

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34
Q

What is the most common anaemia in hospital patients

A

CDA

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35
Q

What chronic infections cause anaemia

A
  1. TB
  2. Crohn’s
  3. Rheumatoid
  4. SLE
  5. Malignancy
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36
Q

Pathophysiology of CDA

A
  1. Decreased release of iron from bone marrow to developing erythroblasts (before they become reticulocytes)
  2. Inadequate erythropoietin response (cytokine which increases RBC production) to anaemia
  3. Decreased RBC survival
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37
Q

Clinical presentation of CDA

A
  1. Fatigue
  2. Headache
  3. Dyspnoea
  4. Angina
  5. Anorexia
  6. Intermittent Claudication
  7. Palpitations
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38
Q

Level of iron and TIBC in CDA

A
  1. LOW TIBC and SERUM IRON
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39
Q

Level of serum ferritin in CDA

A

Normal/ raised due to inflammatory process

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40
Q

Level of transferrin receptors in CDA

A

Normal

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41
Q

Appearance of RBCs in blood count

A
  1. NORMOCYTIC
  2. MICROCYTIC
  3. HYPOCHROMIC
42
Q

How is CDA treated

A

Erythropoietin is effective in raising Hb levels

43
Q

Side effect of treating with erythropoietin in CDA

A

Flu
Hypertension
Rise in platelet count
thromboembolism

44
Q

Main causes of normocytic anaemia

A
  1. ACUTE blood loss
  2. CDA
  3. Endocrine disorders
  4. Renal failure
  5. Pregnancy
45
Q

Clinical presentation of normocytic anaemia

A
  1. Fatigue, headaches, faintness
  2. Dyspnoea
  3. Angina
  4. Anorexia
  5. Intermittend claudication
  6. Palpitations
46
Q

B12 and folate levels in normocytic anaemia

47
Q

Reticulocyte level in normocytic anaemia

48
Q

Hb level in normocytic anaemia

49
Q

Appearance of RBCs in blood count

A

NORMOCYTIC

50
Q

How is normocytic anaemia treated

A
  1. Improve diet with vitamins

2. Erythropoietin injections

51
Q

What can macrocytic anaemia be divided into

A

Megaloblastic

Non-megaloblastic

52
Q

What is megaloblastic macrocytic anaemia

A

Presence of erythroblasts with delayed nuclear maturation because of delayed DNA synthesis - large megaloblastic cells with no nuclei

53
Q

What is non-megaloblastic macrocytic anaemia

A

Erythroblasts are normal

54
Q

Main causes of megaloblastic macrocytic anaemia

A
  1. B12 deficiency

2. Folate deificnecy

55
Q

What is B12 also known as

56
Q

Non-megaloblastic causes of macrocytic anaemia

A
  1. Alcohol
  2. Liver disease
  3. Hypothyroidism
  4. Haemolysis
  5. Marrow failure
  6. Marrow infiltration
  7. Myeloma
57
Q

What kind of anaemia is pernicious anaemia

A

Megaloblastic

58
Q

Where is B12 found

A

Meat
Fish
Dairy

59
Q

Is B12 found in plants

60
Q

How long are body stores of B12

61
Q

How is B12 absorbed

A

Binding to intrinsic factor produced by parietal cells

62
Q

Where is B12 absorbed

A

Terminal ileum

63
Q

What is B12 needed for

A

Thymidine and DNA synthesis

64
Q

Pathophysiology of pernicious anaemia

A

Impairment of DNA synthesis = delayed nuclear maturation

Large RBCs + decreased RBC production in marrow

65
Q

Why is bone marrow most effected in pernicious anaemia

A

As its most active in terms of cell division

66
Q

Why is pernicious anaemia autoimmune

A
  1. Parietal cells are attacked = atrophic gastritis + loss of intrinsic factor production + B12 malabsorption
67
Q

What age group does Pernicious anaemia effect

68
Q

Risk factors for pernicious anaemia

A
  1. Female
  2. Elderly
  3. Fair-heard, blue eyes
  4. Blood group A
  5. Addison’s disease + thyroid
69
Q

Specific diagnosis for pernicious anaemia

A

Intrinsic factor antibodies in blood tests

70
Q

In what proportion of patients can intrinsic factor be found in

A

50% of patients

71
Q

Signs of pernicious anaemia

A
  1. Parietal and chief cells replaced by mucin-decreting cells
  2. Autoimmune gastritis affecting funds with plasma cell + lymphoid infiltration
  3. Achlorhydria (reduced HCL production) + absent of intrinsic factor secretion
  4. Parietal cell antibodies in serum
72
Q

Clinical presentation of pernicious anaemia

A
  1. Normal symptoms for anaemia
  2. Lemon-yellow skin colour
    Red sore tongue + cheilosis
73
Q

Why is skin yellow in pernicious anaemia

A

Caused by ex ess breakdown of haemoglobin (body will try to remove large RBCs that are defective)

74
Q

Neurological features of pernicious anaemia

A
  1. Symmetrical parasthesia in fingers and toes
  2. Weakness + ataxia
  3. Paraplegia
  4. Dementia / hallucinations and optic atrophy from B12 deficiency
75
Q

When do neurological symptoms show in pernicious anaemia

A

Low levels of B12

76
Q

Appearance of RBCs in blood count of pernicious anaemia

A

MACROCYTIC

77
Q

Appearance of microcytes in pernicious anaemia

A
  1. Oval + hyperhsegmented neutrophil polymorphs with 6 or more lobes in nucleus
78
Q

Serum bilirubin levels in pernicious anaemia

79
Q

Why would bilirubin levels in the plasma be raised in pernicious anaemia

A

As a result of ineffective erythropoiesis + increased RBC breakdown

80
Q

What happens to Hb count in pernicious anaemia

81
Q

Reticulocyte count in pernicious anaemia

82
Q

What is the diagnostic factor for pernicious anaemia

A

Low intrinsic factor count

83
Q

How is pernicious anaemia treated

A

Oral B12 - dietary causes

OR IM HYDROXOCOBALAMIN

84
Q

Role of Hydroxocobalamin

A

Replenishes B12 stores

85
Q

Where is folate found

86
Q

Body stores for folate

87
Q

Where is folate absorbed

88
Q

Pathophysiology caused by folate deficiency

A

Impairs DNA synthesis = delayed nuclear maturation

Large RBCs and decreased RBC production in marrow

89
Q

Why is folate essential in fetal development

A

Can result in neural tube defects if deficient

90
Q

Risk factors for folate dificeny anaemia

A

Elderly
Pregnant
Alcohol
Crohn’s or coeliac

91
Q

Clinical presentation for folate deficiency anaemia

A

Same as pernicious EXCEPT no NEUROPATHY

92
Q

How is folate deficiency anaemia diagnosed

A

Same as pernicious except B12 levels should be the same, folate levels should be LOW

93
Q

How is folate deficiency treated

A

Folic acid tablets daily for four months - never without B12

94
Q

Why can’t folate be given without B12

A

Cause degeneration of spinal cord

95
Q

What is haemolytic anaemia

A

Premature breakdown of RBCs, before hitting 120 day lifespan

96
Q

What happens to haemoglobin in renal tubular cells in haemolytic anaemia

A

Broken down and deposited in cells as HAemosiderin

97
Q

Why does shortening red cell survival not equal anaemia all the time

A

Cause compensated increase in RBC production by bone marrow

98
Q

What is compensated haemolytic disease

A

Red cell loss is contained within marrow’s capacity for increased output

99
Q

How does bone-marrow compensate in haemolytic anaemia

A

Increases output by 6-8 times by increasing proportion of cells committed to erythropoiesis (erythroid hyperplasia) + expanding volume of active marrow

Reticulocytes are released PREMATURELY

100
Q

Characteristics of RBCs in haemolytic anaemia

A

MACROCYTIC + stain with a light blue tinge on peripheral blood film

101
Q

Main causes of haemolytic anaemia

A
  1. Hereditary spherocytosis

G6PD deficiency

B Thalassaemia
A Thalassaemia
Sick cell disease

Autoimmune haemolytic anaemia

102
Q

Features of haemolytic anaemia

A
  1. High serum unconjugated bilirubin
  2. High urobilinogen
  3. High fecal stercobilinogen
  4. Splenomegaly
  5. Bone Marrow expansion
  6. Reticulocytosis (more reticulocytes)

Year 2 (155 decks)

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