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BRS/POM MOCKS > POM MOCK 7 - ECM, immune tolerance, anti viral agents > Flashcards

POM MOCK 7 - ECM, immune tolerance, anti viral agents Flashcards

1
Q

What is a the structure of a collagen molecule?

A

Made of 3 alpha chains forming a triple helix.

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2
Q

Why is every third amino acid in collagen glycine?

A

Glycine is the smallest amino acid. Allows for compact structure as it can occupy the interior.

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3
Q

Difference between pro collagen and collagen?

A

Pro collagen has non collagenous domains at n and c termini.

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4
Q

Why is vitamin c required for production of collagen?

A

Vitamin C is required for properly hydroxylated collagen which is needed for cross links. Proline and lysine need hydroxylation.

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5
Q

When is pro collagen converted to collagen?

A

In secretion of fibrillar collagens.

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6
Q

What is required for hydroxylation of collagen once its been secreted?

A

Vitamin C and Fe2+

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7
Q

What forms the cross links in collagen?

A

Lysine and hydroxylysine.

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8
Q

Explain the fibrillar collagen synthesis pathway?

A

Pro alpha chain synthesis. Hydroxylation and glycosylation occurs. Three of these form triple helix. Secretion out of cell. Cleavage of propeptides to form collagen. Assembled into fibril and then into fiber.

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9
Q

What is collagen type IV?

A

Network forming collagen.

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10
Q

What are ehlers–Danlos syndromes (EDS)?

A

Group of inherited connective tissue disorders whose symptoms include stretchy skin and loose joints.

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11
Q

What do fibril associated collagens do? Give an example?

A

Regulate organisation of collagen fibrils. Collagen type IX and XII.

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12
Q

What occurs in Alport syndrome?

A

Mutations in collagen IV result in an abnormally split and laminated glomerular basement membrane.

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13
Q

What are laminins?

A

Role in adhesion. Interacts with integrin and dystroglycan. Made up of alpha,beta and gamma chain.

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14
Q

What links ECM and actin cytoskeleton of cell?

A

Integrins and fibronectin. Fibronectin is bound to collagen and integrin. Integrin binds to actin in cell.

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15
Q

Elastic fibre structure?

A

Elastin core and surrounding microfibrils rich in fibrillin.

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16
Q

Elastin structure?

A

Alternating hydrophillic and hyrophobic domains. Crosslinking of lysine in hydrophillic domains.

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17
Q

Glycosaminoglycan chain structure?

A

Repeating disaccharides.

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18
Q

What can increase the negative charge of GAG chains?

A

Sulfation or carboxylation.

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19
Q

How does aggrecan work?

A

High negative charge. Attracts cations like sodium. Draws in large amounts of water. This resists compressive load.

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20
Q

What cleaves aggrecan?

A

Aggrecanases and metalloproteinases.

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21
Q

What converts a naive t cell to an effector t cell?

A

Antigen recognition. Co-stimulation. Cytokine release.

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22
Q

What cells are involved in resolution and repair after infection is cleared?

A

Macrophages and fibroblasts.

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23
Q

What is central tolerance?

A

Lymphocytes that recognise self antigens are deleted (apoptosis) or made harmless before they enter bloodstream.

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24
Q

What is peripheral tolerance?

A

Destroy or control any self reactive T or B cells which do enter the circulation.

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25
Q

What is negative selection in t cell central tolerance?

A

T cell binds to self mhc too strongly.

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26
Q

What is positive selection in t cell central tolerance?

A

T cell binds to self mhc weakly.

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27
Q

What is death by neglect in t cell central tolerance?

A

T cell doesn’t bind to self mhc.

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28
Q

How can a T cell in the thymus encounter MHC bearing peptides in other parts of the body?

A

Autoimmune regulator gene (AIRE Gene).

29
Q

What is the Autoimmune regulator?

A

Transcription factor that expresses genes from other tissues. This allows T cells to test for self antigens.

30
Q

Mutations in autoimmune regulator gene causes what?

A

Multi organ auto immunity.

31
Q

Why is peripheral tolerance important in relation to b cells?

A

B cells undergo affinity maturation. B cells can turn from non self to self even after leaving maturation in bone marrow.

32
Q

What is anergy (deactivation of t cell)?

A

Type of peripheral tolerance. T cell binding to mhc but antigen presenting cell doesn’t have co stimulation proteins. Engagement of inhibitory receptors on T cell. T cell less likely to be stimulated in the future even if co stimulatory proteins are present.

33
Q

What is ignorance?

A

Type of peripheral tolerance. Antigen is present in too low of a concentration to trigger T cell response.

34
Q

What is antigen induced cell death?

A

Activation of t cell receptor leads to apoptosis. Binding of fas ligand to fas receptor causes apoptosis of t cell.

35
Q

How do Treg cells regulate immune response?

A

Inactivate dendritic cells so naive T cells aren’t activated. Inhibition of T cell effector functions.

36
Q

Treg CD phenotype?

A

CD4 and CD25 present.

37
Q

How do Treg cells regulate immune response if lymphocyte bind to self antigen?

A

T lymphocytes are activated by binding to self antigen on MHC in thymus or peripheral tissues. Activated lymphocytes release IL2. IL2 binds to IL2 receptor on Treg cells and foxp3 is expressed. Release of anti inflammatory cytokines such as IL-10. Inhibition of T cell activation or effector functions.

38
Q

IL-10 function?

A

Anti-inflammatory cytokine. Blocks pro-inflammatory cytokines such as TNF, IL-6, IL-8 and IFN gamma. Downregulates macrophages.

39
Q

Natural regulatory t cells development?

A

Recognition of self antigen during maturation in thymus. Reside in peripheral tissues to prevent harmful reactions against self.

40
Q

Inducible regulatory T cells development?

A

Develop from mature CD4 T cells that are exposed to antigen in the periphery.

41
Q

How do T follicular cells activate B cell?

A

T follicular helper cell binds to MHC II peptide presented by B cell. Release of IL-21 from tfh activates B cell along with the costimulatory proteins.

42
Q

What is a virus?

A

Infectious obligate intracellular parasite.

43
Q

What is an enveloped virus?

A

Lipid bilayer membrane on outermost part of virus.

44
Q

What is a non enveloped virus?

A

Only has a protein caspid on outermost part of virus.

45
Q

Why do RNA and retro viruses lack proof reading capability?

A

They use their own RNA polymerases. These lack proof reading capability.

46
Q

Why do RNA and retro viruses have a higher mutation rate?

A

Lack of proof reading.

47
Q

What does segmentation of viral genome allow?

A

Segmentation of viral genomes allows exchange of intact genes between related viruses when they coinfect the same cell.

48
Q

How does HIV replicate?

A

Binds to CD4 using gp120 receptor. Viral contents enter cell. Viral DNA formed by reverse transcriptase. Viral DNA inserted in human genome using an integrase. New Viral RNA is used as genomic RNA and used to produce viral proteins. New viral RNA and proteins move to cell surface to produce immature HIV. Budds out of cell.

49
Q

How does influenza replicate?

A

Influenza enter cell by endocytosis. Single strand of RNA enters nucleus. RNA is replicated and mRNA is produced. mRNA leaves nucleus and is translated into viral proteins. RNA genomes and viral proteins go to cell surface join together and bud off.

50
Q

What is the cytopathic effect?

A

Morphological changes in cells caused by viral infection

51
Q

What is syncytia?

A

Fusion of multiple cells into a single multinucleated cell body. Viruses can cause this.

52
Q

What technique can be used to detect viral genome?

A

PCR.

53
Q

What technique can be used to detect viral antigen?

A

ELISA.

54
Q

What is acyclovir?

A

Nucleic acid chain terminator. Guanosine derivative.

55
Q

What is acyclovir missing in order to continue addition of nucleotides? What bond can’t be formed?

A

Lack of 3’ -OH prevents phosphodiester bond formation.

56
Q

What allows for the specificity of acyclovir?

A

Only activated inside virus infected cells as it can only be phosphorylated by virus-encoded thymidine kinase present in herpes virus. Higher affinity for viral dna polymerase rather than host cell polymerase.

57
Q

What does remdesivir treat?

A

Hepatitis C and SARS-COV-2

58
Q

How does remdesivir treat hepatitis C?

A

Adenosine derivative. Cause chain termination 3 nucleotides downstream of incorporation by twisting DNA.

59
Q

Amantadine treats what disease?

A

Influenza A.

60
Q

How does amantadine work?

A

Blocks M2 channel protein. Influenza is locked in the endosome as H+ ions can’t enter M2 channel protein and so no uncoating of virus.

61
Q

What has prevented amantadine from working?

A

A single point mutation in the M2 channel protein.

62
Q

What are relenza and tamiflu?

A

Neuraminidase inhibitors.

63
Q

How do neuraminidase inhibitors work?

A

Prevents sialic acid cleavage by inhibiting neuraminidase enzyme. Virus is stuck on cell.

64
Q

What does baloxavir treat and how?

A

Influenza. Inhibits PA endonuclease.

65
Q

HIV antiviral drug mechanisms?

A

Fusion inhibitors, co receptor antagonists, Reverse transciptase inhibitors, integrase inhibitors, protease inhibitors (block maturation stage at end).

66
Q

What is palivizumab?

A

Monoclonal antibody. Type of passive immunotherapy use to treat RSV (Respiratory syncytial virus).

67
Q

What is dexamethasone and tocilizumab

A

Immunomodulators. Dexamethasone is a steroid that decreases inflammatory response and toculizimab inhibits IL-6.

68
Q

Cure for HIV?

A

Transplant of bone marrow from a CCR5 delta 32 donor.

BRS/POM MOCKS (23 decks)

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