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Foundation Of Health and Medical Practice > Haemotology > Flashcards

Haemotology Flashcards

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USMLE® Step 1 flashcards
1
Q

What are the 3 components of blood that can be transfused separately?

A

RBCs, Platelets, Plasma

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2
Q

Define the word hematocrit

A

This is the volume of blood that consists of RBCs.

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3
Q

What does blood plasma consist of?

A

1) Fibrinogen
2) Albumin
3) Immunoglobulins
4) Clotting factors

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4
Q

What are immature RBCs called?

A

Reticulocytes

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5
Q

What makes reticulocytes different to RBCs?

A

Reticulocytes have rRNA.

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6
Q

Name the 2 types of leucocytes

A

1) Granulocytes

2) Monocytes - that then become macrophages, phagocytosis.

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7
Q

What are the 3 granulocytes?

A

1) Neutrophils - remain in tissues and bloodstream for fast action when antigen is recognised.
2) Basophils
3) Eosinophils - mainly part of the type 1 hypersensitivity, degranulation of mast cells.

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8
Q

What are the lymphocytes present in blood?

A

T cells and B cells.

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9
Q

What are platelets?

A

Platelets are cellular fragments from megakaryocytes.

Important for blood clotting and form the platelet plug.

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10
Q

Where are clotting factors, albumin and immunoglobulins produced?

A

These components are made in the liver.

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11
Q

What is the function of albumin in the blood?

A

Involved in maintaining blood osmolality (cannot cross the cell membrane barrier, it is an effective osmole).

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12
Q

How should red blood cells be stored?

A

Stored at 4 degrees up to 35 days.

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13
Q

How should platelets be stored?

A

Stored at 22 degrees and has to be constantly agitated to prevent clumping.
Can only be kept for 7 days due to risk of bacterial infection from high storage temperature.

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14
Q

What is needed to match red blood cells?

A

The blood group and cross match are needed.

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15
Q

What is needed to match platelets?

A

The blood group is needed but crossmatch is not needed.

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16
Q

What is another word for platelets?

A

Thrombocytes

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17
Q

Why are multiple donors and apheresis (cell separation) needed when giving a patient platelets?

A

Apheresis reduces the number of donations a patient is exposed to.

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18
Q

What is fresh frozen plasma?

A

Plasma containing clotting factors that is derived from only one donor.

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19
Q

How is fresh frozen plasma stored?

A

Stored at -30 degrees and can be kept for a year.

Must be thawed 20-30 minutes before use and used quickly so coagulation factors do not degenerate.

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20
Q

What will happen if the thawing temperature of fresh frozen plasma is too hot?

A

The proteins will denature.

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21
Q

What is needed to match fresh frozen plasma?

A

The blood group is needed but cross match is not needed.

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22
Q

What is cryoprecipitate?

A

It is fresh frozen plasma that has been stored at 4-8 degrees overnight.

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23
Q

Why is fresh frozen plasma turned to cryoprecipitate?

A

Proteins with a higher molecular weight are precipitated out. It contains fibrinogen and factor VIII.

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24
Q

What is the genetic relationship between the ABO antigens?

A

A and B are both co dominant alleles.

O is recessive to both alleles.

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25
Q

What are ABO antibodies?

A

These are antibodies that occur in the bloodstream that act against the antigens that the person does not express.

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26
Q

What antibodies are present in a person with an A blood group?

A

B antibodies

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27
Q

What blood group does a person have if they have A and B antibodies in their bloodstream?

A

O blood group

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28
Q

What is the most common blood group in the UK?

A

O+ blood group.

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29
Q

What is the structure of antigens on blood cells?

A

They are glycosylated, so is a monosaccaride attached to a protein by covalent bonding.

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30
Q

When does antibody production occur after birth?

A

Antibodies are produced 3-6 months after birth. (Before that all antibodies are maternal).

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31
Q

Why can’t ABO antibodies cross the placenta?

A

They are IgM antibodies therefore are too large to cross the placenta.

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32
Q

What can happen if the blood groups given do not match?

A

The ABO antibodies can agglutinate and activate complement. This leads to haemolysis of the blood cells which can be fatal.

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33
Q

What is the Rhesus factor?

A

It is an antigen on RBCs that codes for the D antigen.

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34
Q

What determines whether the D antigen is expressed (positive) or not (negative)?

A

Having the D antigen is a dominant trait, so only if heterozygous recessive they will not have the D antigen.

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35
Q

What antibodies are present in those that RhD negative?

A

They have Anti-D antibodies that can develop after being exposed to the D antigen (as an immune response).

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36
Q

Can RhD antibodies cross the placenta?

A

Yes, they are IgG so can pass from the mother to the child (leads to haemolytic disease of the newborn).

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37
Q

Which blood type is the universal donor?

A

O RhD negative blood is a universal donor as the cells have no antigens so will not trigger an immune response from recipients blood.

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38
Q

Which blood type is the universal recipient?

A

AB RhD positive blood is a universal recipient as there are no antibodies in their plasma (universal plasma donor).

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39
Q

What happens if a person with RhD negative blood is exposed to RhD positive blood?

A

Delayed transfusion reaction occurs.
After exposure to RhD antigens, anti-D antibodies are produced.
If the blood is exposed to RhD positive blood in the future the IgG anti-D antibodies will cause haemolysis of those RhD positive blood cells.

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40
Q

When can delayed transfusion reactions be dangerous?

A

In haemolytic disease of the newborn.
If the mother previously was exposed to RhD antigens from a previous birth or blood transfusion, can cause haemolysis to second child if they are RhD positive and mother has anti-D antibodies.
Can be fatal for the foetus.

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41
Q

How can haemolytic disease of the newborn be prevented?

A

Mother can be given artificial anti-D antibodies at birth.
These bind to the foetal RhD positive RBCs, which prevents immunisation so mother doesn’t produce anti-D antibodies herself.
Sensitisation is prevented.

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42
Q

What occurs in acute immune haemolytic transfusion reactions?

A

The donor blood is incompatible with the recipient.

Means the IgM antibodies bind to the donor blood cells and cause activation of complement and haemolysis of RBCs.

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43
Q

List symptoms of acute immune haemolytic transfusion reactions

A

1) Chills/Fever
2) Black urine - due to free haemoglobin
3) Tachycardia
4) Hypotension
5) Chest pain
6) Hot sensation in transfused region

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44
Q

What is the treatment for acute immune haemolytic transfusion reactions?

A

1) Stop transfusion
2) Give fluids if hypotensive
3) Catheterise due to renal failure.
4) Ionotropic support and hemofiltration.
5) Send transfused blood back to lab to check for the error.

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45
Q

What are non immune transfusion reactions caused by?

A

Bacteria, Viruses, Prions

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46
Q

What is caused as a result of non immune transfusion reactions?

A

Sepsis - bacteria are directly entering the bloodstream.

Iron overload as this can deposit in organs and cause heart failure.

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47
Q

How can iron overload treated in those with non immune transfusion reactions?

A

Iron chelators can be used to prevent iron overdose.

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48
Q

What is the biggest cause of transfusion errors?

A

Mistakes in transfusing the incorrect blood components = human error.

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49
Q

When would the patients blood be irradiated before a blood transfusion?

A

If the patient has reduced T cell function (post bone marrow transplant).
This reduces the risk of Graft Vs Host disease.

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50
Q

What is Graft Vs Host disease?

A

Occurs when T cells from transplanted stem cells or bone marrow attack own body cells.

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51
Q

Why would CMV negative blood be required in a transfusion?

A

The blood will not produce antibodies for CMV.

Important for patients with underdeveloped immune systems, pregnant or in intensive care.

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52
Q

How can formation of red cell alloantibodies be prevented?

A

Other blood group systems not only the ABO system is matched to the donor blood.

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53
Q

When are transfusions always given?

A

1) In major haemorrhage

2) Gastro intestinal bleeding

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54
Q

What are alloantibodies?

A

Antibodies formed when exposed to an incompatible blood group.

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55
Q

What is the purpose of the Direct Antiglobulin Test?

A

This test detects antibodies that are already present on patient’s RBCs.
In vivo.

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56
Q

Outline what happens in the Direct Antiglobulin Test

A

Antiglobulin is added to patients red blood cells with antibodies already attached.
Causes RBC aggregation, which shows that the specific antibody is present on those cells.

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57
Q

What is the purpose of the Indirect Antiglobulin Test?

A

This test detects antibodies present in the blood of the patient.
In vitro.

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58
Q

Outline what happens in the Indirect Antiglobulin Test?

A

Patient’s serum is added to a test of red blood cells and anti globulin is added.
If there is agglutination it indicates the patient has antibodies against the antigens on the test of red blood cells.

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59
Q

Define serum

A

A plasma sample that has not clotted.

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60
Q

What is anaemia?

A

When the number of RBCs or the carrying capacity of O2 is insufficient to meet physiological needs.

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61
Q

Define pancytopenia

A

Decreased RBC
Decreased WBC
Decreased platelet count

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62
Q

Define thrombocytopenia

A

Decreased platelet count

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63
Q

Define leukocytopenia

A

Decreased WBC count

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64
Q

Where are red blood cells produced?

A

In the bone marrow, from haematopoietic stem cells.

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65
Q

When red blood cells mature, how does the staining colour change?

A

Changes from deep blue to red/pink.

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66
Q

Name the chemical released from the kidneys that increases RBC production

A

Erythropoietin

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67
Q

In what conditions does the kidney release erythropoietin?

A

When there is lack of oxygen saturation.

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68
Q

What are the 4 subunits of haemoglobin?

A

2 alpha and 2 beta globin chains.

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69
Q

What part of the haemoglobin allows the binding of oxygen?

A

The haemolytic group, which contains iron.

This is bound by a porphyrin ring.

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70
Q

What is activated by the receptors that bind to erythropoietin that proliferates RBCs?

A

The JAK2 transducer

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71
Q

How are RBCs adapted to moving through capillaries?

A

1) Biconcave shape
2) Membrane flexibility
3) Compliance

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72
Q

Outline the death of haemoglobin

A

1) Globin part is broken down on the white blood cell to amino acids. Can then be used for protein synthesis.
2) Haem group is extracted and enters the circulation. There it binds to transferrin. This forms ferritin. This is then used for more RBCs (if no iron then no RBCs can be made).
3) Porphyrin ring is broken down into bilirubin.

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73
Q

Where do RBCs die?

A

In the reticulo-endothelial system, spleen and liver.

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74
Q

How is the Hb level in a patient determined?

A

1) Sample taken through venepuncture.
2) Sample placed in an automated blood count analyser.
3) All Hb cells are lysed and photometric method directly measures level of Hb.
4) Expressed in g/L.

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75
Q

Define the Mean Cell Volume (MCV)

A

This is the size of the RBCs (expressed in fL 10^-15)

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76
Q

Define Red Cells Distribution (RDW)

A

This is a measure of the variance of red blood cell size as a percentage.

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77
Q

Why can the reticulocyte count be important?

A

Shows if the bone marrow is producing enough RBCs.

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78
Q

What type of anaemia is present if the MCV is below 80fL?

A

Microcytic anaemia

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79
Q

What type of anaemia is present when the MCV is higher than 100fL?

A

Macrocytic anaemia

80
Q

What type of anaemia is preset if the MCV is around normal levels?

A

Normocytic anaemia

81
Q

What are the features of a microcytic iron deficiency anaemia blood film?

A

1) Pale coloured RBCS
2) Pencil Cells
3) Hypochromatic cell - darker coloured nucleus
4) Variation in RBC shape
5) Variation in size

82
Q

What are the features of a sickle cell anaemia blood film?

A

1) Sickle shaped RBCs
2) Polychromasia - increased reticulocytes
3) Nucleated erythrocytes - ineffective erythropoiesis
4) Hypersegmented neutrophils
5) Howell-Jolly bodies

83
Q

What are the features of macrocytic magaloblastic anaemia blood film?

A

1) Large RBCs
2) Hypersegmented neutrophils
3) Oval macrocytes
4) Howell-Jollybodies

84
Q

Why does G6PD deficiency cause anaemia?

A

G6PD helps protect RBCs from oxygen radicals so that they can work. A deficiency in this will cause RBCs to break down, thereby causing haemolytic anaemia.

85
Q

What are the features of a G6PD anaemia blood film?

A

1) Keratocytes - “bite” taken out of cells
2) Fewer RBCs
3) Polychromatic macrocytes

86
Q

What are the features of an autoimmune haemolytic anaemia blood film?

A

1) Polychromasia - increased reticulocytes

2) Spherocytes - loss of membrane causes more flexible RBCs

87
Q

What are the features of microcytic thalassaemia anaemia blood film?

A

1) Hyperchromic - RBCs have more haemoglobin so a deeper colour
2) Nucleated RBCs - ineffective erythropoiesis

88
Q

List the 3 main reasons for anaemia

A

1) Excessive RBC loss
2) Insufficient /abnormal RBC production
3) Excessive RBC destruction

89
Q

What conditions can cause excessive RBC loss?

A

1) Menorrhagia
2) Surgery trauma
3) Haematuria - blood in urine
4) Internal bleeding

90
Q

What conditions can cause insufficient/abnormal RBC production?

A

1) Haematinic deficiency - deficiency of nutrients needed for RBC production.
2) Iron deficiency
3) Reduced globin chain production of haemoglobin
4) Bone marrow failure - WBC ingest the iron that is needed
5) Kidney failure/disease - insufficient erythropoietin production so cannot produce RBCs.

91
Q

What conditions can cause excessive RBC destruction?

A

1) Inherited immune defects - RBC membrane defect, Hb defect
2) Autoimmune disease - can be caused by infection and drugs
3) Mechanical heart valves
4) Micro angiopathic disorders, can cause haemolysis

92
Q

Describe the symptoms of anaemia

A

Excessive fatigue, dyspnoea, tachycardia, insomnia, dizziness.

93
Q

Describe the use of a full blood count to investigate anaemia

A

Can be used to see the quantity of each individual component of the blood eg. reticulocytes count, MCV etc

94
Q

Describe the use of haematinics to investigate anaemia

A

Can see the levels of ferritin, B12 and folate in the blood. This can help see what the specific cause of the anaemia is.

95
Q

What happens to the bilirubin concentration if the patient has haemolysis?

A

The bilirubin conc will increase due to the destruction of RBCs increasing.

96
Q

What happens to the LDH concentration in the blood if haemolysis increases?

A

Level of LDH will increase as haemolysis means LDH will not be contained in the cells so the LDH conc in the blood will increase.

97
Q

What happens to the haptoglobin concentration if there is haemolysis?

A

Level of haptoglobin will decrease as its function is to remove free haemoglobin.
In haemolysis there lots of free haemoglobin so more haptoglobin will be bound to haemoglobin.

98
Q

Which nutrients are needed for RBC production?

A

B12, Folate, Iron

99
Q

What is the RBC distribution width?

A

Indicates the variation of the size of the RBCs.
Normal = uniform RBCs
Increased = RBCs are different sizes

100
Q

What is ferritin?

A

A protein that stores iron.

101
Q

What is transferrin?

A

Glycoprotein responsible for the transport of iron in the blood.

102
Q

What is the Total Iron Binding Capacity?

A

The amount of iron needed to saturate the plasma transferrin by binding to it.

103
Q

What is the full blood count for microcytic iron deficiency anaemia?

A

TIBC -> Will be increased as not enough iron present in the blood to bind to transferrin.

Transferrin saturation -> Decreased due to less iron

104
Q

How is the full blood count different in iron deficiency anaemia and anaemia of chronic disease?

A

The TIBC of anaemia of chronic disease is low, in iron deficiency the TIBC is high.

105
Q

How does the transferrin saturation change for microcytic thalassaemia from iron deficiency?

A

The transferrin saturation increases, in iron deficiency it decreases.

106
Q

What is the main cause of megaloblastic anaemia?

A

B12 or folate deficiency

107
Q

How does B12/folate deficiency cause anaemia?

A

Leads to abnormal DNA synthesis and abnormal cell formation.

108
Q

What is a specific type of megaloblastic anaemia?

A

Pernicious anaemia

109
Q

What is pernicious anaemia?

A

It is an autoimmune disease where the parietal cells that secrete acid in the stomach are damaged.
This means B12 cannot be absorbed, resulting in B12 deficiency.

110
Q

What is the main indicator of pernicious anaemia?

A

Beefy red tongue and all blood cell counts being lowered.

111
Q

Why does a high reticulocyte count occur during blood loss?

A

The body is trying to compensate for the blood loss by producing more immature red cells.

112
Q

What is the difference in the full blood count of acute and chronic blood loss?

A

In chronic anaemia the MCV decreases, in acute anaemia the MVC does not change.

113
Q

What is the cause of sickle cell anaemia?

A

A mutation in the beta globulin chain of haemoglobin, causing an abnormal haemoglobin to form.
These chains are more rigid at low pO2, so they clump together.
Causes haemolysis of the sickle cells.

114
Q

Why is it inappropriate to treat iron deficiency anaemia with iron?

A

Accumulation of iron can be toxic.

115
Q

Why does the platelet count increase in iron deficiency?

A

Increase in RBC production in the bone marrow. (To compensate for lack of RBCs).

116
Q

Why does the platelet count decrease in B12 and folate deficiency?

A

No DNA synthesis due to deficiency of B12 and folate, so less platelets can be produced in the first place.

117
Q

What is coagulation?

A

This is the control of bleeding that is activated when blood vessel walls are injured, and due to infection or inflammation.

118
Q

What is haemostasis?

A

This is the name of the process of control bleeding in vessels and allowing the vessel to be repaired.

119
Q

What is the role of the Von Willebrand Factor in primary haemostasis coagulation?

A

It acts as a molecular anchor and allows platelets in blood to adhere to the damaged vascular endothelium.

120
Q

Where are clotting factors released from?

A

They are released from granules that are released from platelets adhering to the vascular endothelium.

121
Q

How do blood clots dissolute?

A

Fibrinolysis occurs to cause dissolution of the clot so that the vessel can be repaired.

122
Q

What is primary haemostasis?

A

The first reaction to damage to blood vessels.
When bleeding is not severe.
Only involves platelet aggregation and adhesion.

123
Q

What cells are platelets formed from?

A

They are formed from megakaryocytes.

These are found in the bone marrow.

124
Q

What initiates platelet aggregation when the vessel is damaged?

A

Exposure of collagen of the blood vessel initiated primary haemostasis.

125
Q

What is the Von Willebrand Factor a carrier molecule for?

A

It is a carrier molecule for factor VIII.

126
Q

What is the disease caused by deficiency of factor VIII?

A

Haemophilia A

127
Q

Which factor is deficient in Haemophilia B?

A

Factor IX

128
Q

What is similar about the type of disease of Haemophilia A and B?

A

They are both X linked recessive genetic diseases.

129
Q

What is secondary haemostasis?

A

It is the activation of the coagulation cascade that leads to the formation of the platelet plug through fibrin formation.

130
Q

What is the function of fibrinogen?

A

It allows inter-platelet bridging between platelets, which provides a platform for coagulation.

131
Q

What are the names or the 2 pathways involved in coagulation?

A

The intrinsic and extrinsic pathway.

132
Q

What is the name of the pathway that the extrinsic and intrinsic pathway both feed into?

A

The final common pathway.

133
Q

Which coagulation pathway occurs first?

A

Extrinsic

134
Q

What activates the extrinsic pathway?

A

Tissue damage

135
Q

What activates the intrinsic pathway?

A

Blood vessel damage (can only occur after tissue damage).

136
Q

Outline the extrinsic pathway

A

1) Trauma to the body causes tissue factors to be exposed.
2) This activates factor VII.
3) Activation to factor VIIa causes activation of factor X directly and activation of factor IX indirectly.
4) This then leads to the final common pathway.

137
Q

Where does blood coagulation occur?

A

On the platelet phospholipid membrane.

138
Q

Outline the final common pathway

A

1) Activated factor Xa combines with factor Va, Ca2+ and phospholipids to from the prothrombinase complex.
2) In the prothrombinase complex prothrombin is activated and produces thrombin.
3) Thrombin converts fibrinogen to fibrin to from a thrombus.
4) The insoluble fibrin is cross linked by factor XIII to stabilise the clot.

139
Q

Outline the intrinsic pathway

A

1) Damage to blood vessels exposes tissue collagen.
2) This activates factor XII -> XIIa.
3) This activates factor XI -> XIa.
4) This activates factor IX -> IXa.
5) This activates factor VIII -> VIIIa.
6) This leads to the activation of factor X.
7) This then leads to the final common pathway.

140
Q

Name 2 tissue collagens that can activate the intrinsic pathway

A

1) Kininogen

2) Kallikrein

141
Q

What are the 3 variables that can activate factor X and the final common pathway?

A

1) Activated factor VIII.
2) Activation of factor VII with tissue factor.
3) Tenase complex - factor VIII and factor IXa in the presence of Ca2+.

142
Q

What is the function of Ca2+ ions in coagulation?

A

Ca2+ ions enable clotting factors to bind to the phospholipid membrane of the platelets.

143
Q

What is factor I?

A

Fibrinogen

144
Q

What is factor Ia?

A

Fibrin

145
Q

What is factor II?

A

Prothrombin

146
Q

What is factor IIa?

A

Thrombin

147
Q

What is factor III?

A

Tissue factor

148
Q

What is factor IV?

A

Ca2+ ions

149
Q

Which 4 factors depend on Vitamin K?

A

Factor II, VII, IX, X

150
Q

What is the function of Vitamin K?

A

Vitamin K is a cofactor for gamma carboxylation of the clotting factors.

151
Q

What happens when deficient in Vitamin K?

A

Clotting factors II, VII, IX and X are unable to be fully formed so cannot attach to platelets and be part of the coagulation cascade.
Results in excessive bleeding as the blood clot is unable to form.

152
Q

Give an example of an anticoagulant that does not occur naturally in the body

A

Warfarin

153
Q

How does Warfarin work?

A

Warfarin inhibits the enzyme that regenerates Vitamin K (epoxide reductase).
Means that factor II, VII, IX and X cannot fully form so cannot bind to the platelet membrane.
Results in blood clotting being inhibited.

154
Q

How does Heparin work?

A

Heparin accelerates natural antithrombin inhibition.
It activates Protein C which inhibits factor Va and factor VIIIa. This in turn prevents formation of factor X, so no thrombin is produced.
Protein S is a cofactor of Protein C.

155
Q

In what form is Warfarin administered?

A

Tablet

156
Q

In what form is Heparin administered?

A

Injection

157
Q

Give an example of a natural anticoagulant effect in the body

A

Tissue Factor Pathway Inhibitor

158
Q

How does the Tissue Factor Pathway Inhibitor work?

A

It prevents the Tissue Factor forming a complex with factor VIIa in the extrinsic pathway, and prevents the Tissue Factor forming a complex with factor VIIIa and factor X.
Means that factor X is not activated so no thrombin can be formed.

159
Q

The activity of which molecule causes fibrinolysis?

A

Plasmin

160
Q

Where is plasmin produced from?

A

It is produced from plasminogen.

Its release is initiated by Tissue Plasminogen Activator (tPA) and Urokinase (uPA).

161
Q

Where is the Tissue Plasminogen Activator (tPA) synthesised?

A

It is synthesised and secreted by the vascular endothelium.

162
Q

Name the main inhibitor of the tissue plasminogen activator

A

Plasminogen Activator Inhibitor - 1

163
Q

What is a product of fibrinolysis that can be used to diagnose DVT and PE?

A

D-dimer, which is cross linked.

164
Q

Outline how PFA-100 is used to test any defects of primary haemostasis

A

Uses membranes coated with agonists of platelet aggregation.

The bleeding time measured is the length of time taken for those membranes to close.

165
Q

What are 3 diseases that could result in a prolonged bleeding time?

A

1) Thrombocytopenia
2) Platelet function defect
3) Von Willebrand Factor disease

166
Q

What is thrombocytopenia?

A

When there is an insufficient number of platelets.

167
Q

Name 3 causes of thrombocytopenia

A

1) Failure to produce platelets from the bone marrow
2) Increased destruction of platelets - autoimmune diseases
3) Increased use of platelets - in haemostasis in sepsis

168
Q

What is an intramuscular haematoma?

A

Where there is bleeding into the muscles and severe disturbance to platelets.

169
Q

What is splenomegaly?

A

When there is a large number of platelets present in the spleen.

170
Q

What is petechiae?

A

They are purple spots indicating bleeding into the skin.

171
Q

What is purpura?

A

It is a larger haemorrhage into the skin.

172
Q

Name some symptoms of thrombocytopenia

A

1) Easy bruising
2) Epistaxes
3) Menorrhagia
4) Purpura
5) Petechiae

173
Q

Which pathway does Prothrombin Time measure?

A

The extrinsic pathway

174
Q

If there is a prolonged Prothrombin Time which clotting factors have been affected?

A

Factors VII, X, V, II (Prothrombin), I (Fibrin)

175
Q

Name 3 causes of a prolonged Prothrombin Time

A

1) Liver disease - coagulation factors are synthesised here.
2) Vitamin K deficiency - Vitamin K is needed for factors II, VII, IX and X. Can be caused by Warfarin therapy.
3) Big blood transfusion - dilutes the number of platelets so fewer clotting factors.

176
Q

What does Thrombin Time measure?

A

Time taken for thrombin to convert fibrinogen to fibrin.

177
Q

Name 2 causes of prolonged Thrombin Time

A

1) Use of Heparin - increases antithrombin inhibition

2) Liver disease

178
Q

Which pathway does Activated Partial Thromboplastin Time measure?

A

The intrinsic pathway

179
Q

if there is a prolonged APTT which factors have been affected?

A

Factors XII, XI, IX, VII, X, V, II, I.

180
Q

Which is the only factor not measured by the APTT that is in the intrinsic pathway?

A

Factor XIII

181
Q

Name 4 causes of a prolonged APTT

A

1) Liver diseases
2) Warfarin therapy
3) Vitamin K deficiency
4) Massive blood transfusions
5) Heparin therapy

182
Q

Which is more prevalent, Haemophilia A or Haeomphilia B?

A

Haemophilia A is more prevalent

183
Q

What would be the result of the APTT, PT and TT test for someone with Haemophilia A or B?

A

The PT and TT would be a normal result.

The APTT would be prolonged as factor VIII and IX are both in the intrinsic pathway.

184
Q

What is prophylactic recombinant factor a treatment for?

A

It is a treatment for Haemophilia.

185
Q

What are the 2 forms of Von Willebrand Factor disease?

A 
Autosomal dominant (mild disease)
Autosomal recessive (severe disease)
186
Q

Why does Von Willebrand Factor disease prolong the APTT time?

A

Because it is a carrier for factor VIII, which is present in the intrinsic pathway.
Deficiency of vWF means a deficiency in factor VIII.

187
Q

What is a deep vein thrombosis?

A

This occurs when there is too much clotting in the deep veins of the leg.

188
Q

Which is more at risk of a deep vein thrombosis, the proximal limb or distal limb?

A

There is a greater risk of DVT in the proximal limb rather than the distal limb.

189
Q

What is a pulmonary embolism?

A

When a thrombus becomes dislodged and reaches the lungs via the circulation.
Can cause problems with breathing.

190
Q

Define thromboprophylaxis

A

This is when treatment is administered in order to reduce the risk of a venous thromboembolism.

191
Q

What are 3 variables that increase the risk of a deep vein thrombosis occurring?

A

1) Stasis - the stopping of the normal flow of bodily fluid
2) Hypercoagulability - tendency for coagulation cascade to occur more
3) Vessel wall injury

192
Q

How does thrombophilia cause hypercoagulability?

A

Tendency towards thrombosis due to deficiency of antithrombin, protein C or protein S. This increases the risk of thrombosis.

193
Q

How can a mutation in factor V cause hypercoagulability?

A

The mutation in factor V is resistant to protein C inactivation.

194
Q

How can anti phospholipid syndrome cause thrombosis?

A

Antibodies are formed that can predispose an individual to thrombosis.

195
Q

List risk factors of thrombosis

A 
Pregnancy
Dehydration
Obesity
Surgery
Cancer
Contraceptive pill

Foundation Of Health and Medical Practice (8 decks)

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