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Phase 1 > CVR: Haematology > Flashcards

CVR: Haematology Flashcards

1
Q

When blood is put in a centrifuge, the buffy coat is the very small layer in between the haematocrit and the plasma.

What components of blood would you find in the buffy coat?

A

Platelets and leucocytes.

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2
Q

Oncotic pressure is the osmotic pressure generated by large molecules in the blood. What is the main blood component that causes oncotic pressure?

A

Large proteins such as albumin.

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3
Q

How does plasma help regulate temperature?

A

Plasma acts as a heat sink to stabilise overall body temperature. Moves excess heat from “hot” organs e.g. liver and muscle, and circulates to extremities.

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4
Q

How do proteins buffer hydrogen ions in the plasma, to help maintain normal pH?

A

Acidic conditions: amino acids bond to H+
Alkaline conditions: amino acids release H+

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5
Q

What is complement (AKA complement system/complement cascade)?

A

A specialised series of proteins that contribute towards the inflammatory response.

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6
Q

What are the three pathways in the complement system?

A

Classical pathway
Alternative pathway
Lectin pathway

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7
Q

Which complement pathway is initiated by specific sugars on the surface of microbes?

A

Lectin pathway

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8
Q

Why does the alternative pathway in complement cascade occur faster than the classical pathway?

A

It takes time for WBCs to create antibodies, which the classical pathway requires for activation.
Where as the alternative pathway is activated directly by pathogens or damaged cells.

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9
Q

What is opsonisation?

A

A process by which opsonins such as complement proteins or antibodies coat pathogens to enhance their recognition and ingestion by phagocytes.

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10
Q

What are the main three functions of complement?

A

Opsonisation.
Cell lysis.
Chemotaxis (causing inflammation by attracting immune cells to site).

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11
Q

Where are plasma proteins such as albumin, complement, and clotting factors produced?

A

In the liver.

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12
Q

What is haemostasis?

A

Normal blood clotting in response to an injury.

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13
Q

What are the three pathways of the coagulation cascade?

A

Intrinsic, extrinsic, and common.

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14
Q

What is the coagulation cascade?

A

Series of enzymatic reactions that lead to the formation of a stable blood clot.

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15
Q

How is the intrinsic pathway of the coagulation cascade triggered?

A

Damage to the vascular endothelium exposes collagen, which activates Factor XII, starting cascade.

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16
Q

The intrinsic pathway of the coagulation cascade begins with activation of Factor XII. What other factors are involved in the intrinsic pathway, until activation of Factor X in the common pathway?

A

XII -> XIIa -> XI -> XIa -> IX
IX and VIIIa then both activate Factor X in common pathway.

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17
Q

How is the extrinsic pathway of the coagulation cascade triggered?

A

External trauma causing Tissue Factor (TF) to be released from damaged tissue.

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18
Q

The extrinsic pathway of the coagulation cascade begins with Tissue Factor release.

What other factors are involved in the extrinsic pathway, until activation of Factor X in the common pathway?

A

Tissue Factor combines with Factor VIIa, activating Factor X in common pathway.

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19
Q

Which coagulation cascade pathway is faster, intrinsic or extrinsic? Why?

A

Extrinsic pathway is faster. Fewer steps and clotting factors involved!

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20
Q

What is the convergent point for both intrinsic and extrinsic pathways in the coagulation cascade?

A

Factor X - the start of the common pathway.

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21
Q

What is the first step of the common pathway of the coagulation cascade?

A

Activated factor X + factor Va converts prothrombin (factor II) to thrombin (factor IIa).

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22
Q

What are the two main roles of thrombin in the common pathway of the coagulation cascade?

A

Converts fibrinogen (factor I) to fibrin.
Activates factor XIII.

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23
Q

How does fibrin and Factor XIII help form a clot?

A

Fibrin forms a mesh over the platelet plug, strengthening it and forming a stable clot.
Factor XIII cross-links fibrin to further strengthen the clot.

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24
Q

How does antithrombin III affect the coagulation cascade?

A

Inhibits thrombin and Factors IXa, Xa, XIa, and XIIa.

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25
Q

What inactivates Factors Va and VIIIa to slow down coagulation cascade?

A

Protein C and Protein S

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26
Q

Does Tissue Factor Pathway Inhibitor (TFPI) inhibit the extrinsic or intrinsic pathways of the coagulation cascade?

A

Extrinsic - blocks Tissue Factor VIIa complex.

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27
Q

What is fibrinolysis?

A

Breakdown of fibrin by a cascade of proteolytic enzymes.

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28
Q

What is the function of tissue plasminogen activator (tPA) in fibrinolysis?

A

Acts as an enzyme to convert plasminogen into its active form plasmin, which dissolves fibrin clots.

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29
Q

Platelets are small, anucleate cell fragments.

What cells are platelets derived from?

A

Megakaryocytes in the bone marrow, which produce multiple platelets from one cell.

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30
Q

How long do platelets live for?

A

7-10 days.

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31
Q

In haemostasis, platelets form a platelet plug, and work with fibrin to form a stable clot.
What are three other functions of platelets?

A
  1. Attract other platelets and clotting factors.
  2. Release growth factors for wound healing.
  3. Trigger inflammation.
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32
Q

How are platelets activated?

A

Damage to blood vessel endothelium exposes collagen.
Platelets stick to exposed collagen and release chemical signals that activate more platelets.

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33
Q

How do platelets form a plug (platelet aggregation)?

A

When platelets are activated e.g. by collagen, they change shape from smooth discoid to spiky stellate. Stick to each other like velcro, and bond together chemically.

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34
Q

What percentage of blood volume is erythrocytes (haematocrit)?

A

45%

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35
Q

Why do erythrocytes have a biconcave shape?

A

To increase the surface area for gaseous exchange.

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36
Q

What is the diameter of an erythrocyte?

A

10 mircometres

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37
Q

Where are erythrocytes produced?

A

In the bone marrow.

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38
Q

The Bohr shift is a shift to the right of the oxygen affinity curve. In what conditions does the Bohr shift occur?

A

The Bohr shift occurs in conditions when there is higher demand for O2 in the tissues.

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39
Q

What affect does the Bohr shift have on the haemoglobin affinity for O2?

A

The Bohr shift is a shift to the right on the oxygen affinity curve, which means haemoglobin have reduced affinity for O2, so more O2 is released to tissues.

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40
Q

How is 2,3-DPG produced?

A

Produced by erythrocytes during glycolysis, in the Luebering-Rapoport Pathway.

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41
Q

What triggers an increase in production of 2,3-DPG?

A

Factors associated with increased tissue O2 demand e.g. hypoxia, anaemia, low pH.

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42
Q

2,3-DPG reduces the affinity of haemoglobin for O2, promoting release of O2 into tissues. Briefly explain the process by which 2,3-DPG reduces haemoglobin affinity for O2.

A

2,3-DPG reduces the co-operative binding effect of haemoglobin, by stabilising the low O2 binding state and preventing O2 from changing the shape of haemoglobin to increase affinity.

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43
Q

What has a higher affinity for O2, myoglobin (Mb), foetal haemoglobin (HbF), or adult haemoglobin (HbA)?

A

Myoglobin in muscle has the highest affinity for O2!
Both HbF and Mb have higher affinity for O2 than HbA, so can “steal” O2 from HbA.

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44
Q

What is carbaminohaemoglobin?

A

CO2 bound to haemoglobin. One route by which CO2 is transported in the blood.

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45
Q

In erythrocytes, CO2 is converted to bicarbonate/HCO3- by carbonic anhydrase. How does the HCO3- then leave the erythrocytes to travel in plasma?

A

HCO3- is transported out of the erythrocyte in 1:1 ratio with Cl- to maintain neutral charge. This is the chloride shift.

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46
Q

Where does reverse chloride shift occur?

A

In the pulmonary capillaries.

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47
Q

Name two important functions of the chloride shift.

A
  1. Increases venous blood carrying capacity of CO2.
  2. Mitigates the change in pH that would otherwise occur in peripheral circulation due to metabolic byproducts (mainly CO2).
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48
Q

CO2 is transported in the blood in three different forms. What are they?

A
  1. HCO3-
  2. Carbaminohaemoglobin
  3. CO2, directly dissolved in plasma
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49
Q

How long does erythropoiesis take?

A

3 weeks.

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50
Q

Where is erythropoietin produced?

A

In the kidneys.

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51
Q

Surface changes, such as damage, on erythrocytes signal to macrophages in the spleen and liver to destroy them. What is this process called?

A

Erythrophagocytosis.

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52
Q

What is the most common leucocyte?

A

Neutrophils.

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53
Q

Neutrophils are involved in the initial immune response (innate immunity). Name two functions neutrophils perform to defend the body.

A

Phagocytose pathogens.
Release cytokines to promote inflammation and activate other leucocytes.

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54
Q

What are Natural Killer (NK) cells?

A

Natural Killer cells destroy virus-infected cells and tumour cells.

55
Q

Which leucocytes are involved in adaptive immunity?

A

B and T lymphocytes.

56
Q

What are the three main types of leucocytes? Give specific cell-type examples of each.

A

Granulocytes (neutrophils, eosinophils, and basophils)
Monocytes (macrophages, dendritic cells)
Lymphocytes (T cells, B cells, Natural Killer Cells)

57
Q

What is the lifespan of neutrophils?

A

5-90 hours.

58
Q

What 2 different cells can B cells differentiate into when activated by an antigen?

A

Plasma cells that produce antibodies.
Memory cells which retain immunity.

59
Q

What are immunoglobulins?

A

Glycoprotein molecules produced by plasma cells (differentiated B cells) in response to an antigen. E.g. IgG, IgM.

60
Q

How long does it take to produce IgM/IgG immunoglobulin response?

A

Around 4 days.

61
Q

Why is IgM important?

A

It’s the first antibody produced in response to an infection and is effective at activating complement.

62
Q

Where might you find IgA and what is its role?

A

In mucosal areas e.g. digestive and respiratory tracts. Protects mucous membranes.

63
Q

Which is the most abundant antibody in extracellular fluid?

A

IgG.

64
Q

What immunoglobulin is involved in allergic responses and defence against parasitic infections?

A

IgE.

65
Q

Which immunoglobulins activate complement?

A

IgG and IgM.

66
Q

Immunoglobulins clump pathogens together so phagocytes can find them easily. What term describes this function?

A

Agglutination.

67
Q

How are immunoglobulins involved in Antibody-Dependent Cellular Cytotoxicity?

A

Immunoglobulins (antibodies) bind to infected cells. Natural Killer cells to bind to the antibodies and destroy the infected cell.

68
Q

What is the function of neutralising antibodies?

A

Neutralisation; antibodies bind to site of pathogens that is needed to infect healthy cells, which prevents the pathogens entering healthy cells.

69
Q

Where are T cells produced?

A

In the bone marrow, but mature in the thymus.

70
Q

What are CD4+?

A

Helper T cells, assist other immune cells e.g. B cells

71
Q

What are CD8+

A

Cytotoxic T cells, directly kill infected or abnormal cells.

72
Q

What is the key function of regulatory T cells (Tregs)?

A

Help suppress inappropriate immune responses and maintain immune tolerance.

73
Q

Natural Killer cells destroy virus-infected and cancer cells by releasing secretory granules that induce apoptosis.

What are the two toxins in these secretory granules, and how do they work together?

A

Perforin and granzymes.

Granzymes are proteases, enter target cell through pores formed by perforin.

74
Q

Which is the largest leucocyte?

A

Monocytes.

75
Q

What do monocytes differentiate into?

A

Macrophages and dendritic cells.

76
Q

Monocytes play a role in chronic inflammation, but what is their main function in immune response?

A

Phagocytosis of pathogens.

77
Q

Eosinophils are involved in the inflammatory response, and can be raised in asthma. Considering another function of eosinophils, name a different pathology that may cause raised eosinophils.

A

Parasitic infection!
Eosinophils kill parasites by releasing toxic granules.

78
Q

Which is the least common leucocyte?

A

Basophils.

79
Q

What similar functions do eosinophils and basophils have?

A

Both are involved in allergic reactions and inflammation, and help defend against parasites.

80
Q

Name three antigen presenting cells.

A

B cells, macrophages, dendritic cells.

81
Q

Which leucocytes are granulocytes?

A

Basophils, eosinophils, neutrophils.

82
Q

Which leucocytes are agranulocytes?

A

Lymphocytes and monocytes.

83
Q

What cell do all granulocytes differentiate from?

A

Myeloblasts.

84
Q

Why is the oxygen affinity curve non-linear?

A

Because of co-operative binding. When O2 binds to haemoglobin, it changes shape which increases affinity to bind more O2.

85
Q

In the Luebering-Rapoport pathway, biphosphoglycerate mutase catalyses the reaction of 1,3 Biphosphoglycerate into 2,3 Biphosphoglycerate.

What happens to this enzyme in conditions where tissues have high O2 demand?

A

.
Biphosphoglycerate mutase is preferentially active in conditions where tissues have high O2 demand to increase 2,3 DPG production.

86
Q

MHC Class I and MHC Class II are both antigen-presenting molecules.
Do antigens presented by MCH Class I or MHC Class II generally originate from inside the presenting cell?

A

MHC Class I. activates cytotoxic T cells (CD8+), which directly kill infected cells via apoptosis.

87
Q

MHC Class I and MHC Class II are both antigen-presenting molecules.

Antigens presented by which MHC Class molecules activate helper T cells (CD4+), causing them to release cytokines?

A

MHC Class II

88
Q

MHC Class I molecules can present self-antigens or antigens from viruses infecting the presenting cell.

What affect do antigens from viruses presented by MHC Class I molecules have?

A

Activates cytotoxic T cells (CD8+) which then directly kill infected cells by apoptosis.

89
Q

What is the most rare blood group in ABO?

A

The 5th group: Bombay group.

90
Q

What does a blood group depend on?

A

Antibodies in plasma and antigens on erythrocyte cell surface.

91
Q

Why is ABO the main identifying blood type used?

A

ABO is extremely immunogenic. Very unusual in that even if never exposed to other blood types, you still have antibodies against them.

92
Q

What sort of antibodies are A and B antibodies?

A

Mix of IgG and IgM

93
Q

Which blood group is a universal recipient and why?

A

Group AB, because plasma does not contain either anti-A or anti-B antibodies.

94
Q

Which blood group is a universal donor and why?

A

Group O, because does not contain A or B antigens on RBC surface.

95
Q

What two conditions can Rhesus D cause?

A

Haemolytic transfusion reactions.
Haemolytic Disease of the Foetus and Newborn (HDFN).

96
Q

Will a person who is RhD-ve have antibodies against RhD in their plasma if they have never been exposed to Rh+ve blood?

A

No, only will develop RhD antibodies after being exposed by blood transfusion or after pregnancy with a Rh+ve baby.

97
Q

When is RhD immunoglobulin, known as anti D, given to pregnant women and why?

A

Prior to delivery, or after sensitising event, and again if baby is confirmed Rh+ve. Given to prevent formation of RhD antibodies

98
Q

In reverse typing, agglutination (cells clumping together in a line on top of gel in tube) signifies a positive test. What does this mean?

A

Occurs when the sample serum has reacted to the test antigen, demonstrating serum has antibodies to the test erythrocyte ABO type.

99
Q

In forward typing, agglutination (cells clumping together in a line on top of gel in tube) signifies a positive test. What does this mean?

A

Occurs when the sample red cells have reacted to the test serum antibodies, demonstrating sample erythrocytes have antigens to the test antibody.

100
Q

What is cross-matching?

A

The intended donor RBCs are combined with the recipient’s serum to see if reaction occurs (indirect Coombs test).

101
Q

When might a direct Coombs test performed?

A

If a transfusion reaction has occurred.

102
Q

What is apheresis in blood donation?

A

Blood removed and externally separated into plasma and platelets. RBCs are returned to donor.

103
Q

Why is plasma from female patients who have donated blood thrown away?

A

Female plasma is thought to be more immunogenic.

104
Q

What is the shelf life of donated RBCs?

A

35 days.

105
Q

What is the shelf-life of platelets?

A

7 days.

106
Q

What are the four potential transfusion reactions?

A

Haemolytic reactions.
Bacterial contamination.
Transfusion-related lung injury (TRALI).
Transfusion-associated circulatory overload (TACO).

107
Q

A blood donor is blood group AB. Recipients with which ABO blood group can be given their packed red blood cells?

A

AB only.

108
Q

Why can Type O patients only be given Type O blood?

A

Type O have antibodies to both A and B in plasma so can only receive Group O blood (which has neither A or B antigens).

109
Q

Why do platelets change their shape when activated?

A

To increase surface area which increases the possibility of cell-cell interactions.

110
Q

What receptors on platelets binds them together (platelet aggregation)?

A

Glycoprotein IIb/IIa receptors on different platelets bind with the same fibrinogen molecule.

111
Q

How do platelets adhere to damaged vessel walls?

A

Receptors on the platelet membrane attach to collagen directly or via von Willebrand Factor.

112
Q

Name four agonists that cause platelet activation.

A

Collagen.
Thrombin.
Thromboxane A2.
ADP.

113
Q

What is responsible for synthesising coagulation factors and fibrinogen?

A

The liver.

114
Q

What is the precursor for plasmin?

A

Plasminogen.

115
Q

Describe the coagulation cascade in five words.

A

A series of proteolytic enzymes.

116
Q

What enzyme cleaves fibrinogen to create fibrin?

A

Thrombin.

117
Q

What is released upon platelet activation, containing a high concentration of ADP molecules (which then act as agonists at the platelet P2Y12 receptor)?

A

Platelet dense granules.

118
Q

Name three places von Willebrand factor can be found.

A
  1. Free in plasma.
  2. Inside Weibel-Palade bodies in endothelial cells.
  3. Inside platelet alpha granules.
119
Q

What is the longest protein found in biology?

A

von Willebrand factor!

120
Q

What happens to von Willebrand factor at high shear rates?

A

It unravels from its usual “ball of wool” shape, exposing more sites for platelet binding, and can join together to form nets to catch platelets in.

121
Q

What does the enzymes Cyclooxygenase 1 and 2 (COX 1 & 2) do to arachidonic acid?

A

Both convert arachidonic acid into prostaglandin H2.

122
Q

What prostaglandins are produced by platelets to trigger platelet aggregation and vasoconstriction?

A

Thromboxane A2.

123
Q

What prostaglandins are produced by endothelial cells to cause vasodilation and inhibit platelet aggregation?

A

Prostacyclin.

124
Q

When ADP binds to platelet receptors, it triggers platelet activation causing shape change and platelet aggregation.

What other effect does ADP have on platelets that functions as a positive feedback loop?

A

Triggers platelets to release dense granules, which contain more ADP, into plasma. The ADP can then activate other platelets.

125
Q

Platelets catalyse thrombin generation from prothrombin. Thrombin activates further platelets. What other effect does thrombin have which helps form a stable clot?

A

Thrombin converts fibrinogen into fibrin. Fibrin is needed to stabilise the aggregated platelets into a platelet-fibrin clot.

126
Q

In the fibrinolytic system, what enzyme catalyses plasminogen into plasmin?

A

Tissue plasminogen activator (tPA).

127
Q

In the fibrinolytic system, what enzyme catalyses fibrin into fibrin degradation products (such as D-dimer)?

A

Plasmin.

128
Q

What inhibits tissue plasminogen activator (tPA)?

A

Plasminogen activator inhibitor-1 (PAI-1).

129
Q

What inhibits plasmin by creating inactive plasmin-antiplasmin complex?

A

Antiplasmin.

130
Q

Platelet alpha granules are released into the plasma following platelet activation. What do platelet alpha granules contain?

A

Contain many different proteins; important coagulation factors and inflammatory mediators, including von Willebrand factor and fibrinogen.

131
Q

Platelet alpha granules mediate expression of surface P-selectin on platelet membranes. Why is this important for the inflammatory response?

A

Monocytes can bond to P-selectin, allowing platelets to interact with monocytes.

132
Q

When monocytes bind to platelets via P-selectin, what 3 substances does this trigger monocytes to release?

A
  1. Cytokines (to attract other leucocytes).
  2. Proteolytic enzymes.
  3. Tissue factor.
133
Q

Give an example of an anti-platelet drug that inhibits ADP receptor P2Y12 on platelet membranes.

A

Clopidogrel
OR
Prasugrel
OR
Ticagrelor.

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