PBL Topic 2 Case 7 Flashcards

1
Q

Explain how haemoglobin is involved in the return of CO2 to the lungs

A
  • Contains carbonic anhydrase
  • Allows CO2 to react with H2O
  • To form bicarbonate ions
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2
Q

What does mean corpuscular volume measure?

A
  • Size of red blood cells
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3
Q

What is the normal range of the mean corpuscular volume?

A
  • 80 - 99 femtolitres (fL)
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4
Q

What is the mean diameter, thickness and volume of red blood cells?

A
  • Diameter: 7.8 uM
  • Thickness: 2.5 uM
  • Volume: 90-95 cubic uM
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5
Q

How does the average number of red blood cells differ in males and females?

A
  • Males: 5,200,000

- Females: 4,700,000

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6
Q

What is meant by the term hematocrit?

A
  • Percentage of blood composed of red blood cells
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7
Q

What is the normal value of hematocrit?

A
  • 45 per cent
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8
Q

Where are red blood cells produced in early embryonic life?

A
  • Yolk sac
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9
Q

Where are red blood cells produced during the second trimester?

A
  • Liver
  • Spleen
  • Lymph Nodes
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10
Q

Where are red blood cells produced during the final month of gestation and after birth?

A
  • Bone marrow
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11
Q

In which types of bones does the marrow typically produce red blood cells after birth?

A
  • Membraneous bones

- Including sternum, ribs and vertebrae

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12
Q

What is a pluripotential haematopoietic stem cell?

A
  • Type of cell from which all cells of the circulating blood are derived
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13
Q

What is a committed stem cell?

A
  • Type of cell that differentiates to form other types of cell
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14
Q

What is a CFU-E?

A
  • Colony-Forming-Unit Erythrocyte

- A committed stem cell that produces erythrocytes

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15
Q

What is a CFU-GM?

A
  • Colony-Forming-Unit Granulocyte and Monocyte

- A committed stem cell that produces granulocytes and monocytes

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16
Q

Identify factors that affect the formation of growth and differentiation inducers in erythrocytes

A
  • Exposure to low oxygen in the blood
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17
Q

Identify factors that affect the formation of growth and differentiation inducers in lymphocytes

A
  • Exposure to a pathogen in the blood
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18
Q

What is CFU-M?

A
  • Colony-Forming-Unit Megakaryocyte

- A committed stem cell that produces platelets

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19
Q

What is the role of erythropoietin?

A
  • Stimulates proliferation of erythrocyte progenitor cells

- Stimulates their differentiation in mature erythrocytes

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20
Q

What is the role of thrombopoeitin?

A
  • Stimulating of megakaryocyte production

- Via its c-mpl receptor

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21
Q

Identify the roles of 3 different colony stimulating factors

A
  • GM-CSF: Increases stem cell commitment to granulocyte and monocyte production
  • G-CSF: Increases stem cell commitment to granulocyte production
  • M-CSF: Increases stem cell commitment to monocyte production
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22
Q

Identify the roles of IL-3, IL-5 and IL-11

A
  • IL-3: Growth and reproduction of all types of stem cells
  • IL-5: Growth and differentiation of eosinophils
  • IL-11: Promotes megakaryocyte production
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23
Q

Identify the role of Stem Cell Factor

A
  • Synergises with IL-3 and GM-CSF

- To increase proliferation of many types of stem cells

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24
Q

Identify the six generations of erythrocytes

A
  • Proerythroblast
  • Basophil Erythroblast
  • Polychromatophil Erythroblast
  • Orthochromatic Erythroblast
  • Reticulocyte
  • Erythrocyte
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25
Q

What occurs during the successive stages of red cell differentiation?

A
  • Accumulation of haemoglobin (B)
  • Nucleus is absorbed (B)
  • Endoplasmic reticulum is absorbed (B)
  • Passage from the bone into the capillaries by diapedesis (R)
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26
Q

Where is erythropoietin produced?

A
  • Kidneys
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27
Q

Explain how erythropoietin stimulates erythropoietic activity?

A
  • Under hypoxic conditions
  • Binds to Hypoxia Inducible Factor
  • Which binds to Hypoxia Response Element
  • Activates gene transcription
  • Via the combined effects of nuclear factor and co-activator p300
  • Increased proportion of committed cells to erythropoiesis
  • Stimulation and differentiation of CFU-E
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28
Q

Explain how under normal conditions HIF is controlled

A
  • The HIF-alpha subunit is hydroxylated
  • Which promotes interaction with von Hippel-Lindau E3 ubiquitin ligase
  • Resulting in degradation of HIF
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29
Q

What is the lifespan of an erythrocyte?

A
  • 120 days
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30
Q

Identify five roles of the cytoplasmic enzymes contained within erythrocytes

A
  • Glucose metabolism
  • Maintain pliability
  • Membrane transport
  • Maintain ferrous iron
  • Prevents oxidation of proteins
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31
Q

What is the role of Kupffer cells?

A
  • Types of macrophages produce by the liver

- Phagocytosis of haemoglobin from worn out red blood cells

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32
Q

What is the role of Transferrin?

A
  • Transport of iron from the haemoglobin from worn out red blood cells to the bone marrow
  • For either production of new red blood cells or storage as ferritin
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33
Q

What happens to the porphyrin portion of the haemoglobin of worn out red blood cells?

A
  • Converted into bilirubin my macrophages

- Removed from the body by secretion through the liver into the bile

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34
Q

Explain how red blood cells may self-destruct in the spleen

A
  • Squeeze through red pulp into the trabeculae
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35
Q

Explain how a molecule of pyrrole is produced in the formation of Haemoglobin

A
  • Succinyl coenzyme A is formed in the Krebs cycle

- It binds with glycine to form Pyrrole

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36
Q

Explain how protoporphyrin IX is produced in the formation of Haemoglobin

A
  • Four molecules of pyrrole combine
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37
Q

Explain how haem is formed formed protoporphyrin IX

A
  • Protoporphyrin IX reacts with ferrous iron (Fe2+)
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38
Q

Explain how a haemoglobin chain is produced from haem

A
  • Haem combines with globulin
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39
Q

Which chains make up Haemoglobin A?

A
  • 2 x Alpha Chain

- 2 x Beta Chain

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40
Q

How many molecules of oxygen can be transported by a molecule of haemoglobin? Why is this the case?

A
  • Four
  • There are four haem group
  • Which contain a single iron atom
  • That can form a loose bond with oxygen
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41
Q

How does the T conformation of haemoglobin differ to the R conformation?

A
  • T: Globin chains are held tight together
  • R: Oxygen binding sites are more exposed
  • Therefore R conformation has a higher affinity for oxygen
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42
Q

Why is haemoglobin considered an allosteric protein

A
  • Binding of one oxygen molecule increases oxygen affinity of the remaining binding sites
  • This explains the sigmoid shape of the oxygen dissociation curve
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43
Q

What is the effect of binding of hydrogen ions and carbon dioxide to haemoglobin?

A
  • Reduced affinity for oxygen
  • Bohr Effect
  • Oxygen dissociation curve shifts right and downwards
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44
Q

What is the effect of oxygenation on haemoglobin?

A
  • Reduced affinity for Carbon Dioxide

- Haldane Effect

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45
Q

What is the effect of 2,3-BPG on haemoglobin?

A
  • Stabilises T-conformation
  • Reduced affinity for oxygen
  • Oxygen dissociation curve shifts right and downwards
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46
Q

Explain the role of ferrireductase

A
  • Conversion of ferric iron (Fe3+) to ferrous iron (Fe2+)
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47
Q

Explain the role of DMT1 (Divalent Metal Transporter)

A
  • Divalent Metal Transporter

- Transports iron across the luminal surface of the mucosal cells in the small intestine

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48
Q

Explain the role of HCP1

A
  • Haem Carrier Protein 1

- Transports haem across the luminal surface of the mucosal cells in the small intestine

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49
Q

Explain the role of FPN-1

A
  • Ferroportin 1
  • Transports iron out of mucosal cell
  • Requires hephaestin
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50
Q

Explain the role of Hepcidin

A
  • Regulation of iron absorption
  • By binding to iron-exporting protein Ferroportin 1
  • Causing its degradation
  • Decreasing iron efflux
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51
Q

What is the role of apotransferrin

A
  • Combines with iron to form transferrin

- Which is transported in the plasma

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52
Q

Identify two locations where iron is deposited

A
  • Liver

- Bone Marrow

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53
Q

Explain how haemoglobin is produced from circulating iron

A
  • Transferrin attaches to surface receptor on erythrocyte
  • Iron is released and transported to mitochondria
  • Iron combines with protoporphyrin to form haem
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54
Q

Explain how iron is stored from circulating iron

A
  • Transferrin attaches to surface receptor on erythrocyte

- Iron combine with apoferritin to form ferritin

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55
Q

How does ferritin differ from hemosiderin

A
  • Ferritin is soluble

- Hemosiderin is insoluble

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56
Q

Identify three causes of iron deficiency

A
  • Blood loss, typically from GI tract
  • Demands of growth and pregnancy
  • Decreased absorption
  • Poor intake
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57
Q

Identify the four generations of granulocytes

A
  • Myeloblast
  • Promyelocyte
  • Myelocyte
  • Metamyelocyte
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58
Q

What are band forms?

A
  • Immediate precursor of mature granulocytes

- With irregular horseshoe shaped nucleus

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59
Q

What is the difference between left and right shift?

A
  • Left shift involves mobilisation of metamyelocytes

- Right shift involves further maturation

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60
Q

Identify five locations in which lymphocytes and plasma cells are produced

A
  • Bone marrow
  • Spleen
  • Thymus
  • Lymph Glands
  • Peyer’s Patches underneath epithelium in gut wall
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61
Q

What is anaemia?

A
  • Reduction in haemoglobin

- Below the reference level for the age and gender of the individual

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62
Q

Identify three types of anaemia, how are they classified?

A
  • Microcytic Anaemia
  • Normocytic Anaemia
  • Macrocytic Anaemia
  • Classified based on MCV
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63
Q

Identify two mechanisms that occur, resulting in an asymptomatic patient of anaemia

A
  • Enhancement of oxygen carrying capacity of blood

- Rise in 2,3-BPG allowing for oxygen dissociation at the tissues

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64
Q

Identify 7 general symptoms of anaemia

A
  • Fatigue
  • Headache
  • Faintness
  • Breathlessness
  • Angina
  • Claudication
  • Palpitations
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65
Q

What is claudication?

A
  • Pain in limb
  • That occurs on exercise
  • Due to obstruction of an artery
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66
Q

Identify 7 signs of anaemia

A
  • Pallor
  • Tachycardia
  • Systolic Flow Murmur
  • Koilonychia (spoon shaped nails)
  • Jaundice
  • Bone deformities
  • Leg ulcers
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67
Q

How can exercise be used to assess the effects of anaemia?

A
  • Exercise causes angina and intermittent claudication
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68
Q

Identify five evaluation tools when a patient presents with a low haemoglobin count

A
  • Red blood cell indices
  • White blood cell count
  • Platelet count
  • Reticulocyte count (as this indicates marrow activity)
  • Blood film
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69
Q

What is meant by the term dimorphic and when may this be seen on a blood film?

A
  • Two populations of red cells are seen
  • In patients with double deficiencies
  • For example iron and folate deficiency in coeliac disease
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70
Q

What is meant by the term poikilocytosis?

A
  • Variation in cell shape

- As demonstrated in microcytic anaemia

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71
Q

What is mean by the term anisocytosis?

A
  • Variation in cell size

- As demonstrated in microcytic anaemia

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72
Q

Identify two methods of obtaining and examining bone marrow

A
  • Aspiration provides a film which can be examined by microscopy
  • Trephine provides a core of bone which is processed on a histological specimen
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73
Q

Identify five components that are assessed when examining bone marrow

A
  • Cellularity
  • Type of erythropoiesis
  • Cellularity
  • Infiltration of marrow e.g. by cancer cells
  • Iron stores
74
Q

What is the most common cause of microcytic anaemia?

A
  • Iron deficiency
  • Chronic disease (Crohn’s)
  • Sideroblastic Anaemia
  • Thalassaemia
75
Q

Identify seven clinical features of microcytic anaemia

A
  • Brittle nails
  • Koilonychia (spoon-shaped nails)
  • Brittle hair
  • Atrophy of the papillae of the tongue
  • Angular stomatitis
  • Dysphagia
  • Glossitis
76
Q

What would a blood count and film show in iron-deficiency anaemia?

A
  • MCV < 80 fL

- Poikilocytosis and Anisocytosis

77
Q

How are serum iron, ferritin, transferrin receptors and iron-binding capacity affected in iron-deficiency anaemia?

A
  • Serum iron is reduced
  • Serum ferritin is reduced
  • Transferrin receptors is increased
  • Total iron-binding capacity is increased
78
Q

How are serum iron, ferritin, transferrin receptors and iron-binding capacity affected in anaemia of chronic disease?

A
  • Serum iron is reduced
  • Serum ferritin is reduced
  • Transferrin receptors are normal
  • Total iron-binding capacity is is reduced
79
Q

Identify two causes of sideroblastic anaemia?

A
  • Inherited as an X-linked disease

- Acquired through myelodysplasia, myeloproliferative disorders or myeloid leukaemia

80
Q

How can Perl’s reaction be used to demonstrate sideroblastic anaemia?

A
  • Accumulation of iron in mitochondria

- Due to disordered haem synthesis

81
Q

What is the treatment for iron-deficiency anaemia?

A
  • Fasted ferrous sulphate
82
Q

What is the treatment of sideroblastic anaemia?

A
  • Withdrawal of alcohol and drugs

- Pyridoxine

83
Q

How are serum iron, ferritin, transferrin receptors and iron-binding capacity affected in sideroblastic anaemia?

A
  • Serum iron is raised
  • Serum ferritin is raised
  • Transferrin receptors are raised
  • Total iron-binding capacity is normal
84
Q

Identify two causes of normocytic anaemia

A
  • Endocrine disorders e.g. hypopituitarism, hypothyroidism

- Haematological disorders e.g. aplastic anaemia, haemolytic anaemia

85
Q

What is a megaloblast?

A
  • Erythroblast with delayed nuclear division
  • Due to defective DNA synthesis
  • Large immature nuclei
86
Q

Identify two causes of megaloblastic macrocytic anaemia

A
  • Vitamin B12 deficiency or abnormal B12 metabolism

- Folic acid deficiency or abnormal folate metabolism

87
Q

What would a blood count and film show in megaloblastic macrocytic anaemia

A
  • MCV > 96 fL
  • Megaloblasts with large immature nuclei
  • Macrocytes with six or seven lobes in the nucleus
88
Q

Outline the pathophysiology of pernicious anaemia

A
  • Replacement of chief cells by mucin-secreting cells
  • Atrophic gastritis
  • Reduced HCl secretion (achlorhydria)
  • Absence of intrinsic factor production
  • Resulting in B12 malabsorption
89
Q

Identify three autoimmune diseases that are associated with Pernicious anaemia

A
  • Thyroid Disease
  • Addison’s Disease
  • Vitiligo
90
Q

Identify the clinical features of pernicious anaemia

A
  • Jaundice and pallor caused be breakdown of haemoglobin
  • Glossitis and angular stomatitis
  • Neurological changes, including polyneuropathy caused by low levels of B12
91
Q

Why is serum bilirubin reduced in pernicious anaemia?

A
  • Ineffective erythropoiesis
92
Q

Identify the treatment for pernicious anaemia

A
  • Intramuscular hydroxocobalamin

OR

  • Oral B12
93
Q

Identify three unwanted effects of intramuscular hydroxocobalamin

A
  • Iron deficiency
  • Hypokalaemia
  • Hyperuricaemia
94
Q

Identify 8 causes of non-megaloblastic macrocytic anaemia

A
  • Pregnancy
  • Alcohol excess
  • Liver disease
  • Reticulocytosis
  • Hypothyroidism
  • Aplastic Anaemia
  • Sideroblastic Anaemia
  • Hydroxycarbamide
  • Azathioprine
  • Cold agglutinins
95
Q

What is aplastic anaemia?

A
  • Pancytopenia with hypocellularity of the bone marrow
96
Q

What is meant by pancytopenia?

A
  • Deficiency of all three cellular components of the blood

- Erythrocytes, leukocytes and platelets

97
Q

What is meant by hypocellularity?

A
  • Reduced number of cells in the bone marrow
98
Q

Outline the pathophysiology of aplastic anaemia

A
  • Reduced number of pluripotential stem cells
  • Due to immune mechanisms
  • Such as activated cytotoxic T cells
99
Q

Identify a genetic cause of aplastic anaemia

A
  • Fanconi’s anaemia

- Due to mutations of BRCA2

100
Q

Outline four drugs that may cause aplastic anaemia

A
  • Cytotoxic: Busulifan, Doxorubicin (Chemotherapy)

- Non-Cytotoxic: Chloramphenicol, Gold and Carbimazole

101
Q

Outline three clinical features of aplastic anaemia

A
  • Bleeding (blood blisters in mouth)
  • Infection
  • Anaemia
102
Q

Why are broad-spectrum antibiotics given in aplastic anaemia?

A
  • To prevent infection
103
Q

Why are transfusions given in aplastic anaemia?

A
  • Pancytopenia
104
Q

When are antithymocyte globulin and cyclosporin prescribed?

A
  • Patients with severe disease over 40
  • Younger patients with severe disease with an HLA-identical sibling donor
  • Patients who do not have severe disease but who are transfusion dependent
105
Q

What is the main cause of haemolytic anaemia?

A
  • Increased destruction of red blood cells
106
Q

What is compensated haemolytic disease?

A
  • Increased red blood cell output from bone marrow
  • By increasing number of cells committed to erythropoiesis
  • Compensates destruction of red blood cells
107
Q

Where does most of the destruction of red blood cels take place?

A
  • Extravascular destrcution
108
Q

Outline the pathophysiology of haemolytic anaemia

A
  • Haemoglobin is oxidised to methaemoglobin
  • Which dissociates into ferrihaem and globulin
  • Ferrihaem binds to haemopexin, or
  • Ferrihaem binds to albumin to form methaemalbumin (seen on Schumm’s test)
109
Q

Outline the pathogenesis of hereditary spherocytosis

A
  • Autosomal dominant condition

- Affecting roughly 1 in 5000

110
Q

Outline the pathophysiology of hereditary spherocytosis

A
  • Defect in erythrocyte structural protein spectrin
  • Increased permeability to sodium
  • Increased active transport of sodium, out of cell
  • Reduced surface-to-volume ratio
  • Cell become spherical
111
Q

How do spherocytes differ to erythrocytes?

A
  • Rigid and less deformable
  • Unable to pass through splenic microcirculation
  • Shorter lifespan
112
Q

Identify five clinical features of spherocytosis

A
  • Jaundice
  • Anaemia
  • Splenomegaly
  • Leg Ulcers
113
Q

Identify the main course of action with spherocytosis and its associated therapies

A
  • Splenectomy

- Appropriate immunisation and lifelong penicillin prophylaxis

114
Q

Briefly describe foetal haemoglobin

A
  • HbF-aa/YY
  • 2 x Alpha Chain
  • 2 x Beta Chain
115
Q

What is BCL IIA and what is its role?

A
  • Zinc finger protein

- Suppresses the Y gene expression of HbF

116
Q

What is Haemoglobin A?

A
  • A2B2

- Comprises 97% of adult Hb

117
Q

What is Haemoglobin A2?

A
  • A2D2

- Comprises 2% of adult Hb

118
Q

What is Haemoglobin F?

A
  • A2Y2
  • HB of foetus
  • Increased in B-thalassaemia
119
Q

What is Haemoglobin H?

A
  • B4
  • Found in a-thalassaemia
  • Biologically useless
120
Q

What is Haemoglobin Barts?

A
  • Y4
  • Comprises 100% of Hb in homozygous a-thalassaemia
  • Biologically useless
121
Q

What is Haemoglobin S?

A
  • a2B2s

- Substitution of valine for glutamine in position 5 of B chain

122
Q

What is Haemoglobin C?

A
  • a2B2c

- Substitution of lysine for glutamic acid in position 6 of B chain

123
Q

What is meant by B0 and B+ and what is their cause?

A
  • In homozygous B-thalassaemia
  • B0 = No B-chain produced
  • B+ = Reduced B-chain produced
  • Caused by point mutations
124
Q

Identify three types of Hb that are present in B-thalassaemia

A
  • HbA2
  • HbF
  • Small amounts of HbA
125
Q

Outline the clinical features of Thalassaemia Minor?

A
  • Carrier state

- Asymptomatic

126
Q

Outline the clinical features of Thalassaemia Intermedia?

A
  • Splenomegaly
  • Leg ulcers
  • Gallstones
127
Q

Outline the clinical features of Thalassaemia Major (Cooley’s Anaemia)

A
  • Bacterial infections
  • Severe anaemia
  • Hepatosplenomegaly, giving rise to thalassaemic facies
  • ‘Hair on end’ appearance of bony trabeculation
128
Q

What is the main cause of a-Thalassaemia

A
  • Gene deletions

- Duplications

129
Q

What is the four gene deletion?

A
  • Hb Barts (Y4)

- Hydrops fetalis

130
Q

What is the three gene deletion?

A
  • HbH (B4)

- Moderate anaemia and splenomegaly

131
Q

What is the two gene deletion?

A
  • HbA (a2B2)

- Microcytosis with mild anaemia

132
Q

What is the one gene mutation?

A
  • HbA (a2B2)

- Very mild anaemia or no anaemia

133
Q

Outline how the pathogenesis of Sickle Syndromes

A
  • Single base mutation of adenine to thymine

- Substitution of valine for glutamic acid

134
Q

In which country is the sickle gene most common?

A
  • Africa
135
Q

Outline the pathophysiology of sickle cell anaemia

A
  • HbS molecules are rigid and take up sickle appearance
  • Lose membrane flexibility due to dehydration
  • Caused by potassium leaving through Gados Channel
  • Resulting in shortened cell survival
  • And impaired passage through the microcirculation
136
Q

Identify five factors that precipitate cell sickling

A
  • Infection
  • Dehydration
  • Cold
  • Acidosis
  • Hypoxia
137
Q

Outline the three clinical syndromes that can occur in Sickle Syndromes

A
  • Homozygous HbSS (most severe)
  • Combined heterozygosity HbSC (intermediate)
  • Heterozygous HbAS (least severe)
138
Q

Explain why dactylitis occurs in sickle cell anaemia

A
  • Pain in hands and feet
  • Due to vaso-occlusion
    • Adhesion proteins such as VCAM-1
  • Trapping of rigid sickle cells
139
Q

Explain why pulmonary hypertension occurs in sickle cell anaemia

A
  • Haemolysis leads to increased cell-free plasma Hb
  • Which consumes NO
  • A vasodilator substance
140
Q

Explain why Acute Chest Syndrome occurs in sickle cell anaemia

A
  • Infections
  • Fat embolism from necrotic bone marrow
  • Pulmonary infarction due to sequestration of sickle cells
141
Q

What does a blood count show in sickle cell anaemia?

A
  • Hb range of 60-80 g/L
142
Q

What does a blood film show in sickle cell anaemia?

A
  • Hyposplenism

- Sickling

143
Q

What does a Sickle Cell Solubility Test show in Sickle Cell anaemia?

A
  • Turbid (cloudy) appearance

- Due to precipitation of HbS

144
Q

Outline the management of Sickle Cell anaemia

A
  • Prophylactic penicillin and vaccination
  • Blood transfusions
  • Inhaled nitric oxide
  • Stem cell transplantation
145
Q

Identify three causes of acquired haemolytic anaemias

A
  • Autoantibodies
  • Drug-induced antibodies
  • Alloantibodies
146
Q

What are warm agglutinins?

A
  • Autoantibodies that react with red blood cells at 37 degrees
  • Typically IgG
147
Q

What are cold agglutinins?

A
  • Autoantibodies that react with red blood cells at less than 37 degrees
  • Typically IgM
148
Q

What are agglutinogens?

A
  • Antigens on the surface of red blood cells

- Either type A or type B

149
Q

What is type O?

A
  • When neither A or B agglutinogens are present
150
Q

What is type A?

A
  • When only type A agglutinogens are present
151
Q

What is type B?

A
  • When only type B agglutinogens are present
152
Q

What is type AB?

A
  • When both type A and B agglutinogens are present
153
Q

What blood type is a person who has the genotype OO?

A
  • Type O
154
Q

What blood type is a person who has the genotype OA or AA?

A
  • Type A
155
Q

What blood type is a person who has the genotype OB or BB?

A
  • Type B
156
Q

What blood type is a person who has the genotype AB?

A
  • Type AB
157
Q

List the genes in order of frequency from most frequent

A
  • O
  • A
  • B
  • AB
158
Q

When do anti-A agglutinins develop?

A
  • When type A agglutinogen is not present
159
Q

When do anti-B agglutinins develop?

A
  • When type B agglutinogens is not present
160
Q

What are agglutinins?

A
  • Gamma globulins produced in the bone marrow and lymph glands
  • That produce IgM or IgG antibodies
161
Q

Identify two occasions in which agglutinins develop

A
  • Food

- Bacteria

162
Q

What occurs when blood is mismatched?

A
  • Agglutinins bind to agglutinin
  • 2 with IgG, 10 with IgM
  • Cells clump together
  • Phagocytosis results in haemolysis
163
Q

What is the difference between the O-A-B system and the Rh system?

A
  • In the Rh system, spontaneous agglutinins almost never occur
  • Person must first be exposed to an Rh antigen before agglutinins cause a significant transfusion reaction
164
Q

Identify the six types of Rh factors

A
  • C
  • D
  • E
  • c
  • d
  • e
165
Q

What is the relationship between CDE and cde

A
  • A person has either a CDE or a cde
166
Q

Which Rh antigen is most prevalent?

A
  • D
167
Q

What is meant by the term Rh positive?

A
  • A person possessing the D antigen
168
Q

How does the percentage of Rh positive individuals differ in white and black populations?

A
  • 85% of white people are Rh positive

- 95-100% of black people are Rh positive

169
Q

What is meant by alloimmunisation?

A
  • Immune response

- Against foreign RBC antigens

170
Q

Outline the pathophysiology of of an immediate haemolytic transfusion reaction

A
  • Complement activation by the antigen-antibody reaction
  • Caused by IgM antibodies
  • Leads to rigors, lumbar pain, hypotension and renal failure
171
Q

Outline the pathophysiology of of a delayed haemolytic transfusion reaction

A
  • Secondary immune response
  • Caused by IgG antibodies
  • Anaemia and jaundice
  • Blood film shows spherocytosis and reticulocytosis
172
Q

Identify three documentation errors that may occur prior to a blood transfusion

A
  • Failure to check identify of donor when taking the sample
  • Mislabelling blood sample with wrong name
  • Failure to perform patient identify check before blood is transfused
173
Q

Why may urticarial reactions occur during a blood transfusion?

A
  • Plasma protein incompatibility
174
Q

What is the treatment for a urticarial reaction during a blood transfusion?

A
  • Administration of chlorphenamine

- Slowing or stopping treatment

175
Q

Why may anaphylactic reactions occur during a blood transfusion?

A
  • Anti-IgA in a patient lacking IgA
  • Is mixed with transfused blood containing IgA

-

176
Q

What is the treatment for an anaphylactic reaction during a blood transfusion?

A
  • Adrenaline

- Or chlorphenamine

177
Q

Which viruses are screened and tested for prior to blood transfusion?

A
  • HBV
  • HCV
  • HIV-1
  • HTLV-1
178
Q

Why are patients asked about recent travel prior to giving blood?

A
  • Exclude risk of West Nile Virus

- Which is the causal agent of meningoencephalitis

179
Q

Identify a microorganism that can proliferate in red cell and platelet concentrates

A
  • Yersinia enterocolitica
180
Q

Identify three measures to avoid bacterial contaminates when taking blood

A
  • Donor arm cleaning
  • Diversion of initial collection of samples for testing
  • Bacterial detection system for platelet concentrates
181
Q

Why is each donation test using the TPHA?

A
  • Treponema Palladium Haemagglutination Assay

- Test for syphilis