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BRS/POM MOCKS > POM MOCK 3 - lymphoid tissues, haemostasis, lymphocytes, > Flashcards

POM MOCK 3 - lymphoid tissues, haemostasis, lymphocytes, Flashcards

1
Q

Primary lymphoid organs?

A

Thymus, Bone marrow and foetal liver.

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2
Q

What does ‘repertoire’ mean in immunology?

A

The range of genetically distinct BCRs or TCRs present in a given host.

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3
Q

Where do B cell mature?

A

Start of maturation occurs in bone marrow where B cell progenitor is created. Final maturation occurs in periphery in spleen or lymph nodes.

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4
Q

What is a germinal centre?

A

Anatomically restricted site where B cells undergo mutation and selection to generate high affinity antibodies.

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5
Q

How do naïve T cells enter lymph nodes?

A

Selectin binding to endothelial cells. Switch to integrin binding. Transendothelial migration through high endothelial venule.

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6
Q

What is primary haemostasis?

A

Formation of unstable platelet plug.

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7
Q

What is secondary haemostasis?

A

Formation of stable fibrin mesh.

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8
Q

What is the first way platelets can bind to collagen?

A

Directly using their glycoprotein Ia receptor.

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9
Q

What is the second way platelets can bind to collagen?

A

Indirectly using their glycoprotein Ib receptor to bind to Von Willebrand factor (VWF).

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10
Q

Where is Von Willebrand factor (VWF) found?

A

Produced and released from endothelial cells. Produced in megakaryocytes and released from alpha granules in platelets.

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11
Q

What happens after platelets become activated?

A

They become more rounded and form spicules to encourage platelet-platelet interaction. Contents of platelet granules are also released.

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12
Q

What are released from platelet granules?

A

ADP, fibrinogen and von Willebrand factor.

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13
Q

What else along with content from granules is produced and released from platelets?

A

Thromboxane A2

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14
Q

What does thromboxane A2 do?

A

Vasoconstrictor and aids with platelet aggregation.

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15
Q

What 2 main molecules encourage platelet platelet aggregation?

A

ADP and Thromboxane A2

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16
Q

What receptor does ADP bind to promote platelet aggregation?

A

P2Y12 receptor found on platelets.

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17
Q

What receptor does Thromboxane A2 bind to promote platelet aggregation?

A

Thromboxane A2 receptor

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18
Q

What does fibrinogen do in primary haemostasis?

A

Binds to glycoprotein IIb/IIIa which further activates platelets. Also has a key role in linking platelets together to form a platelet plug.

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19
Q

How is platelet activation and aggregation counterbalanced?

A

Active flow of blood and the release of prostacyclin (PGI2) from endothelial cells; prostacyclin is a powerful vasodilator and suppresses platelet activation, thus preventing inappropriate platelet aggregation.

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20
Q

How does aspirin work as an anti platelet drug?

A

Aspirin inhibits the production of thromboxane A2 by irreversibly blocking the action of cyclo-oxygenase (COX) in platelets, resulting in a reduction in platelet aggregation.

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21
Q

How does clopidogrel work?

A

Blocks P2Y12 Receptor and so ADP can’t bind therefore reducing platelet aggregation.

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22
Q

Which factors require vitamin K?

A

Factors II (prothrombin), VII, IX and X

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23
Q

What factor initiates coagulation?

A

Tissue factor (TF).

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24
Q

What does TF bind to?

A

Factor VIIa.

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25
Q

What does binding of TF do?

A

Activates factors IX,X. This leads to factor II (prothrombin) being converted to small amounts of factor IIa (thrombin).

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26
Q

What do calcium ions do?

A

Aid in binding of activated clotting factors to the phospholipid surfaces of platelets.

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27
Q

What happens in the amplification step?

A

Small amount of thrombin mediates the activation of the co-factors V and VIII, the zymogen factor XI and platelets.

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28
Q

What happens in the propagation phase?

A

Factor XI converts more factor IX to IXa, which in concert with factor VIIIa,amplifies the conversion of factor X to Xa, and there is consequently a rapid burst in thrombin generation which cleaves the circulating fibrinogen (soluble) to form the insoluble fibrin clot.

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29
Q

What are the three main natural anticoagulant molecules?

A

Protein C, Protein S and antithrombin.

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30
Q

What activates protein C?

A

Thrombin binding to thrombomodulin on the endothelial cell surface.

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31
Q

What does activated protein C do?

A

Inactivates factors Va and VIIIa in the presence of a co-factor protein S.

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32
Q

What does antithrombin do?

A

Inactivates thrombin and factor Xa.

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33
Q

What makes antithrombin work?

A

Binding of antithrombin to endothelial cell-associated heparins.

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34
Q

Main anticoagulant drugs?

A

Heparin, Warfarin and direct oral anticoagulants.

35
Q

How does heparin work?

A

Works indirectly by potentiating the action of antithrombin leading to the inactivation of factors Xa and IIa (thrombin).

36
Q

How is heparin administered?

A

Intravenously or by subcutaneous injection.

37
Q

How does warfarin work?

A

Vitamin K antagonist that works by interfering with protein carboxylation. It therefore reduces synthesis of functional factors II, VII, IX and X by the liver.

38
Q

How is warfarin administered?

A

Given as an oral tablet and its anticoagulant effect needs to be monitored by regular blood testing

39
Q

Why does warfarin take longer to take effect compared to heparin?

A

Reduces synthesis of coagulation factors in the liver rather than inhibiting existing factor molecules.

40
Q

How do direct oral anticoagulants work?

A

Directly inhibit either thrombin or factor Xa.

41
Q

What lyses fibrin?

A

Plasmin.

42
Q

What is key for fibrin to be lysed?

A

Both plasminogen and t-PA need to bind to lysine residues on fibrin.

43
Q

Why do plasmin levels need to be regulated?

A

Plasmin isn’t specific for fibrin. They can cause break down fibrinogen, factor Va and VIIIa.

44
Q

What inhibits plasmin?

A

alpha 2 macroglobulin and anti-plasmin.

45
Q

When would thrombolytic agents like t-PA be used?

A

To treat PE or ischaemic stroke.

46
Q

Risks of thromobolytic agents?

A

Bleeding.

47
Q

When would anti-fibrinolytic drugs be used?

A

Trauma, surgical patients and patients with bleeding disorders.

48
Q

Examples of anti-fibrinolytic drugs?

A

Tranexamic acid and aminocaproic acid.

49
Q

How do anti-fibrinolytic drugs work?

A

Competitive inhibition. Bind to plasminogen and so plasminogen can’t bind to fibrin and so fibrin isn’t lysed.

50
Q

When is prothrombin time used?

A

To evaluate extrinsic pathway and common pathway.

51
Q

What factors does pro thrombin test for?

A

VII, X, V, II and fibrinogen.

52
Q

What does recombinant thromboplastin contain?

A

Tissue factor and phospholipids.

53
Q

What pathway does APTT (Activated partial thromboplastin time) test for?

A

Intrinsic and common pathway.

54
Q

What factors does APTT (Activated partial thromboplastin time) test for?

A

XII, XI, IX, VIII, X, V, II and fibrinogen.

55
Q

Difference in preparation of PT and APTT?

A

PT tissue factor is used. APTT a contact activator is used.

56
Q

Prolonged APTT causes?

A

Haemophilia A (Factor VIII deficiency). Haemophilia B (Factor IX deficiency). Haemophilia C (Factor XI deficiency)

57
Q

Increased bleeding causes?

A

Thrombocytopenia. Use of anti platelet drugs (e.g aspirin). Reduction in coagulation factors. Increased fibrinolysis (Use of t-PA).

58
Q

3 principle causes of thrombosis (Virchow’s triad)

A

Stasis of blood flow (veins). Endothelial injury (artery). Hyper-coagulability (both).

59
Q

Causes of thromobosis?

A

Inherited thrombophilia (reduced levels of anticoagulant proteins such as antithrombin). Reduced fibrinolytic activity (seen in pregnancy). Hyperviscocity (polycthaemia).

60
Q

How do B cell recognise antigens?

A

Recognise structural 3D epitopes - native antigens.

61
Q

How do T cells recognise antigens?

A

Recognise linear epitopes that are peptides derived from proteins processed by APC’s

62
Q

What happens when lymphocyte receptor binds to antigen?

A

Leads to activation of cell and clonal expansion which results in differentiated effector cells of that lineage that bear the same receptor.

63
Q

What generates the diverse b cell repertoire?

A

Immunoglobulin gene rearrangement. DNA is rearranged before transcription.

64
Q

Explain production of BCR receptor chain?

A

Each BCR receptor chain is encoded by separate multigene families on different chromosomes. During B cell maturation these gene segments are rearranged and brought together. Transcription of B cell DNA then occurs. RNA is then spliced and mRNA is translated to produce polypeptide for that chain that will make up part of the B cell receptor.

65
Q

Where are MHC I peptides processed?

A

Cytosol.

66
Q

Where are MHC II peptides processed?

A

Endosomes.

67
Q

What class of T helper cell would be involved in a viral and intracellular bacteria infections?

A

Th1.

68
Q

What immune cells would be seen in a viral/intracellular bacterial infection?

A

CD8 T cells, NK cells, Th1 cells, neutrophils and macrophages.

69
Q

What immune cells would be seen in a parasitic infection such as a helminth?

A

Eosinophils, basophils, Th2 cells, B cells and macrophages.

70
Q

What immune cells would be seen in an extracellular bacterial infection or fungal infection?

A

Th17, neutrophils and macrophage.

71
Q

T reg role and cytokines?

A

IL-10 and TGF beta.

72
Q

Th1 role and cytokines?

A

Boosts cellular immune response. IF gamma, TNF and IL-12.

73
Q

Th2 role and cytokines?

A

Pro allergic. IL-4, IL-5 and IL-13.

74
Q

Th17 role and cytokines?

A

Pro Inflammatory (controls bacterial and viral infection). IL-17, IL-23 and IL-6.

75
Q

Tfh role and cytokines?

A

Pro antibody. Produces the cytokine IL-21 which drives B cell proliferation.

76
Q

Where are t follicular helper cells found?

A

Secondary lymphoid organs in b cell zones.

77
Q

How does CD8 T cells kill infected cells?

A

Apoptosis. Released perforin which polymerise and form pores in the pathogen cell membrane, then released granzymes through pore that create a cascade that leads to apoptosis by fragmentation of nuclear DNA.

78
Q

What are the 3 functions of antibodies?

A

Neutralisation, Opsonization and complement activation.

79
Q

What class of antibody do thymus independent antigens stimulate production of?

A

Induce IgM synthesis by B cells.

80
Q

What class of antibody do thymus dependent antigens stimulate production of?

A

All Ig-classes.

81
Q

What do thymus independent antigens not stimulate?

A

They do not stimulate immunological memory.

82
Q

How do thymus independent antigens activate B cell?

A

B cell receptor binds to repetitive structure present on bacterial surface. Second signal provided by PAMP such as LPS which binds to toll like receptor on b cell.

83
Q

Explain thymus dependent antigen pathway?

A

B cell ingest pathogen and antigen is internalised and degraded into peptides. Displays antigen peptides on its b cell receptor. DC ingests pathogen and displays peptides on MHC II. CD4 T cell that has complementary TCR to antigen gets activated by DC cell. T helper cell then activated B cell by costimulation and cytokines. B cell turns into plasma cell and produces antibodies for that antigen.

BRS/POM MOCKS (23 decks)

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