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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 -> XI -> IX
Activated IX & VIII 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

Tissue factor (III) is expressed on the surface of many cells found outside blood vessels but not on the surface of circulating blood cells or the endothelium. When the endothelium is damaged, tissue factor comes into contact with blood.

How does this start the extrinsic pathway, and how does this then lead to activation of factor X in the common pathway?

A

Tissue factor combines with Factor VII, which then activates 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 V convert 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 and many other factors, providing a positive feedback loop in the intrinsic pathway.

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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 (IIa) and activated factors IX to XII.

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25
What inactivates Factors V and VIII to slow down coagulation cascade?
Protein C and Protein S
26
Does Tissue Factor Pathway Inhibitor (TFPI) inhibit the extrinsic or intrinsic pathways of the coagulation cascade?
Extrinsic - blocks Tissue Factor VIIa complex.
27
What is fibrinolysis?
Breakdown of fibrin by a cascade of proteolytic enzymes.
28
What is the function of tissue plasminogen activator (tPA) in fibrinolysis?
Acts as an enzyme to convert plasminogen into its active form plasmin, which dissolves fibrin clots.
29
Platelets are small, anucleate cell fragments. What cells are platelets derived from?
Megakaryocytes in the bone marrow, which produce multiple platelets from one cell.
30
How long do platelets live for?
7-10 days.
31
In haemostasis, platelets form a platelet plug, and work with fibrin to form a stable clot. What are three other functions of platelets?
1. Attract other platelets and clotting factors. 2. Release growth factors for wound healing. 3. Trigger inflammation.
32
How are platelets activated?
Damage to blood vessel endothelium exposes collagen. Platelets stick to exposed collagen and release chemical signals that activate more platelets.
33
How do platelets form a plug (platelet aggregation)?
When platelets are activated, they change shape from smooth discoid to spiky stellate. Stick to each other like velcro, and bond together chemically.
34
What percentage of blood volume is erythrocytes (haematocrit)?
45%
35
Why do erythrocytes have a biconcave shape?
To increase the surface area for gaseous exchange.
36
What is the diameter of an erythrocyte?
10 mircometres
37
Where are erythrocytes produced?
In the bone marrow.
38
The Bohr shift is a shift to the right of the oxygen affinity curve. In what conditions does the Bohr shift occur?
The Bohr shift occurs at low pH (which occurs when there is higher demand for O2 in the tissues).
39
What is the Bohr shift?
The Bohr shift is a shift to the right on the oxygen affinity curve due to low pH. A shift to the right means haemoglobin have reduced affinity for O2, so more O2 is released to metabolically active tissues.
40
How is 2,3-DPG produced?
Intermediate product of glycolysis in erythrocytes, in the Luebering-Rapoport Pathway.
41
What triggers an increase in production of 2,3-DPG?
Factors associated with increased tissue O2 demand (hypoxia, anaemia, high altitude).
42
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.
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.
43
What has a higher affinity for O2, myoglobin (Mb), foetal haemoglobin (HbF), or adult haemoglobin (HbA)?
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.
44
What is carbaminohaemoglobin?
CO2 bound to haemoglobin. One route by which CO2 is transported in the blood.
45
In erythrocytes, CO2 is converted to HCO3- (bicarbonate) and H+ by carbonic anhydrase. How does the erythrocyte transport HCO3- out of the cell into plasma, but still maintain neutral charge?
HCO3- is transported out of the erythrocyte and Cl- is transported into the erythrocyte in a 1:1 ratio to maintain neutral charge. This is chloride shift (AKA the Hamburger effect).
46
Where does reverse chloride shift occur?
In the pulmonary capillaries.
47
Name two important functions of the chloride shift.
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).
48
CO2 is transported in the blood in three different forms. What are they?
1. HCO3- 2. Carbaminohaemoglobin 3. CO2, directly dissolved in plasma
49
How long does erythropoiesis take?
3 weeks.
50
Where is erythropoietin produced?
In the kidneys.
51
Surface changes, such as damage, on erythrocytes signal to macrophages in the spleen and liver to destroy them. What is this process of destruction called?
Erythrophagocytosis.
52
What is the most common leucocyte?
Neutrophils.
53
Neutrophils are involved in the initial immune response (innate immunity). Name two functions neutrophils perform to defend the body.
Phagocytose pathogens. Release cytokines to promote inflammation and activate other leucocytes.
54
What are Natural Killer (NK) cells?
Natural Killer cells destroy virus-infected cells and tumour cells.
55
Which leucocytes are involved in adaptive immunity?
B and T lymphocytes.
56
What are the three main types of leucocytes? Give specific cell-type examples of each.
Granulocytes (neutrophils, eosinophils, and basophils) Monocytes (macrophages, dendritic cells) Lymphocytes (T cells, B cells, Natural Killer Cells)
57
What is the lifespan of neutrophils?
5-90 hours.
58
What 2 different cells can B cells differentiate into when activated by an antigen?
Plasma cells that produce antibodies. Memory cells which retain immunity.
59
What are immunoglobulins?
Glycoprotein molecules produced by plasma cells (differentiated B cells) in response to an antigen. E.g. IgG, IgM.
60
How long does it take to produce IgM/IgG immunoglobulin response?
Around 4 days.
61
What is the first antibody produced in response to an infection, and is also effective at activating complement?
IgM.
62
Where might you find IgA and what is its role?
In mucosal areas e.g. digestive and respiratory tracts. Protects mucous membranes.
63
Which is the most abundant antibody in extracellular fluid?
IgG.
64
What immunoglobulin is involved in allergic responses and defence against parasitic infections?
IgE.
65
Which immunoglobulins activate complement?
IgG and IgM.
66
Immunoglobulins clump pathogens together so phagocytes can find them easily. What term describes this function?
Agglutination.
67
How are immunoglobulins involved in Antibody-Dependent Cellular Cytotoxicity?
Immunoglobulins (antibodies) bind to infected cells. Natural Killer cells to bind to the antibodies and destroy the infected cell.
68
What is the function of neutralising antibodies?
Reducing ability of pathogens to cause further infection. This is called neutralisation; antibodies bind to site of pathogens that is needed to infect healthy cells, which prevents the pathogens entering healthy cells.
69
Where are T cells produced?
In the bone marrow, but mature in the thymus.
70
What are CD4+?
Helper T cells, assist other immune cells e.g. B cells
71
What are CD8+
Cytotoxic T cells, directly kill infected or abnormal cells.
72
What is the key function of regulatory T cells (Tregs)?
Help suppress inappropriate immune responses and maintain immune tolerance.
73
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?
Perforin and granzymes. Granzymes are proteases, enter target cell through pores formed by perforin.
74
Which is the largest leucocyte?
Monocytes.
75
What do monocytes differentiate into?
Macrophages and dendritic cells.
76
Monocytes play a role in chronic inflammation, but what is their main function in immune response?
Phagocytosis of pathogens.
77
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.
Parasitic infection! Eosinophils kill parasites by releasing toxic granules.
78
Which is the least common leucocyte?
Basophils.
79
What similar functions do eosinophils and basophils have?
Both are involved in allergic reactions and inflammation, and help defend against parasites.
80
Name three antigen presenting cells.
B cells, macrophages, dendritic cells.
81
Which leucocytes are granulocytes?
Basophils, eosinophils, neutrophils.
82
Which leucocytes are agranulocytes?
Lymphocytes and monocytes.
83
What cell do all granulocytes differentiate from?
Myeloblasts.
84
Why is the oxygen affinity curve non-linear?
Because of co-operative binding. When O2 binds to haemoglobin, it changes shape which increases affinity to bind more O2.
85
In the Luebering-Rapoport pathway, biphosphoglycerate mutase catalyses the reaction of 1,3 Biphosphoglycerate into 2,3 Biphosphoglycerate (2,3 DPG). What happens to this enzyme in conditions where tissues have high O2 demand?
. Biphosphoglycerate mutase is preferentially active in conditions where tissues have high O2 demand to increase 2,3 DPG production.
86
MHC Class I and MHC Class II are both antigen-presenting molecules. Which of these two molecules are found on most nucleated cells, and present pathogenic antigens to cytotoxic T cells (CD8+), causing them to kill the cell?
MHC Class I.
87
MHC Class I and MHC Class II are both antigen-presenting molecules. Which of these two types are found only on antigen-presenting cells, and present pathogenic antigens to helper T cells (CD4+), causing them to release cytokines?
MHC Class II.
88
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?
Activates cytotoxic T cells (CD8+) which then directly kill infected cells by apoptosis.
89
What is the most rare blood group in ABO?
The 5th group: Bombay group.
90
What does a blood group depend on?
Antibodies in plasma and antigens on erythrocyte cell surface.
91
Why is ABO the main identifying blood type used?
ABO is extremely immunogenic. Very unusual in that even if never exposed to other blood types, you still have antibodies against them.
92
What sort of antibodies are A and B antibodies?
Mix of IgG and IgM
93
Which blood group is a universal recipient and why?
Group AB, because plasma does not contain either anti-A or anti-B antibodies.
94
Which blood group is a universal donor and why?
Group O, because does not contain A or B antigens on RBC surface.
95
What two conditions can Rhesus D cause?
Haemolytic transfusion reactions. Haemolytic Disease of the Foetus and Newborn (HDFN).
96
Will a person who is RhD-ve have antibodies against RhD in their plasma if they have never been exposed to Rh+ve blood?
No, only will develop RhD antibodies after being exposed by blood transfusion or after pregnancy with a Rh+ve baby.
97
When is RhD immunoglobulin, known as anti D, given to pregnant women and why?
Prior to delivery, or after sensitising event, and again if baby is confirmed Rh+ve. Given to prevent formation of RhD antibodies
98
In reverse typing, agglutination (cells clumping together in a line on top of gel in tube) signifies a positive test. What does this mean?
Occurs when the sample serum has reacted to the test antigen, demonstrating serum has antibodies to the test erythrocyte ABO type.
99
In forward typing, agglutination (cells clumping together in a line on top of gel in tube) signifies a positive test. What does this mean?
Occurs when the sample red cells have reacted to the test serum antibodies, demonstrating sample erythrocytes have antigens to the test antibody.
100
What is cross-matching?
The intended donor RBCs are combined with the recipient's serum to see if reaction occurs (indirect Coombs test).
101
When might a direct Coombs test performed?
If a transfusion reaction has occurred.
102
What is apheresis in blood donation?
Blood removed and externally separated into plasma and platelets. RBCs are returned to donor.
103
Why is plasma from female patients who have donated blood thrown away?
Female plasma is thought to be more immunogenic.
104
What is the shelf life of donated RBCs?
35 days.
105
What is the shelf-life of platelets?
7 days.
106
What are the four potential transfusion reactions?
Haemolytic reactions. Bacterial contamination. Transfusion-related lung injury (TRALI). Transfusion-associated circulatory overload (TACO).
107
A blood donor is blood group AB. Recipients with which ABO blood group can be given their packed red blood cells?
AB only.
108
Why can Type O patients only be given Type O blood?
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
Why do platelets change their shape when activated?
To increase surface area which increases the possibility of cell-cell interactions.
110
What receptors on platelets binds them together (platelet aggregation)?
Glycoprotein IIb/IIa receptors on different platelets bind with the same fibrinogen molecule.
111
How do platelets adhere to damaged vessel walls?
Receptors on the platelet membrane attach to collagen directly or via von Willebrand Factor.
112
Name four agonists that cause platelet activation.
Collagen. Thrombin. Thromboxane A2. ADP.
113
What is responsible for synthesising coagulation factors and fibrinogen?
The liver.
114
What is the precursor for plasmin?
Plasminogen.
115
Describe the coagulation cascade in five words.
A series of proteolytic enzymes.
116
What enzyme cleaves fibrinogen to create fibrin?
Thrombin.
117
What is released upon platelet activation, containing a high concentration of ADP molecules (which then act as agonists at the platelet P2Y12 receptor)?
Platelet dense granules.
118
Name three places von Willebrand factor can be found.
1. Free in plasma. 2. Inside Weibel-Palade bodies in endothelial cells. 3. Inside platelet alpha granules.
119
What is the longest protein found in biology?
von Willebrand factor!
120
What happens to von Willebrand factor at high shear rates?
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
What do the enzymes Cyclooxygenase 1 and 2 (COX 1 & 2) do to arachidonic acid?
Both convert arachidonic acid into prostaglandin H2.
122
What prostaglandins are produced by platelets to trigger platelet aggregation and vasoconstriction?
Thromboxane A2.
123
What prostaglandins are produced by endothelial cells to cause vasodilation and inhibit platelet aggregation?
Prostacyclin.
124
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?
Triggers platelets to release dense granules, which contain more ADP, into plasma. The ADP can then activate other platelets.
125
Platelets catalyse thrombin generation from prothrombin. Thrombin activates further platelets. What other effect does thrombin have which helps form a stable clot?
Thrombin converts fibrinogen into fibrin. Fibrin is needed to stabilise the aggregated platelets into a platelet-fibrin clot.
126
In the fibrinolytic system, what enzyme catalyses plasminogen into plasmin?
Tissue plasminogen activator (tPA).
127
In the fibrinolytic system, what enzyme catalyses fibrin into fibrin degradation products (such as D-dimer)?
Plasmin.
128
What inhibits tissue plasminogen activator (tPA)?
Plasminogen activator inhibitor-1 (PAI-1).
129
What inhibits plasmin by creating inactive plasmin-antiplasmin complex?
Antiplasmin.
130
Platelet alpha granules are released into the plasma following platelet activation. What do platelet alpha granules contain?
Contain many different proteins; important coagulation factors and inflammatory mediators, including von Willebrand factor and fibrinogen.
131
Platelet alpha granules mediate expression of surface P-selectin on platelet membranes. Why is this important for the inflammatory response?
Monocytes can bond to P-selectin, allowing platelets to interact with monocytes.
132
When monocytes bind to platelets via P-selectin, what 3 substances does this trigger monocytes to release?
1. Cytokines (to attract other leucocytes). 2. Proteolytic enzymes. 3. Tissue factor.

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