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Pharm Y2S1 > Immunology > Flashcards

Immunology Flashcards

1
Q

What is innate immunity?

A

Non specific first line defence system- physiological barriers, inflammatory defence, phagocytosis

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2
Q

What are the two subtypes of myeloid cells?

A

Granulocytic- neutrophils, basophils, eosinophils

Monocytic- macrophages, langerhans, kupffer, dendritic

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3
Q

What are the two types of lymphoid cells?

A

T cells

B cells

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4
Q

What are monocytes?

A

Type of white blood cell, larger than lymphocytes.

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5
Q

What are the characteristic components of monocytes?

A

Horse shoe shaped nucleus

Faint azurophilic granules

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6
Q

What are macrophages?

A

Antigen presenting cells that increase levels of phagocytosis when stimulated.

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7
Q

What are neutrophils?

A

Largest and most abundant white blood cells, important in bacterial destruction.

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8
Q

What are basophils?

A

Deep violet granules release histamine and bind complements C3a, C3b and C5a. Small numbers in circulation

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9
Q

What are eosinophils?

A

Gather at site of parasitic/allergic reaction and release toxins.

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10
Q

What are NK cells?

A

Bind to infected cells/macrophages and kill them along with the phagocytosed microbes.

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11
Q

What are mast cells?

A

Release factors that increase blood flow and vascular permeability to bring immunity components to site of infection.

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12
Q

What is adaptive immunity?

A

Slow activation but specific memory. Vary response depending on microorganism.

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13
Q

What is the main role of CD4+ T helper cells?

A

Recognise antigens presented on class II major histocompatibility complexes.

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14
Q

What do category I T helper cells do?

A

Stimulate cell mediated immunity

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15
Q

What do category II T helper cells do?

A

Stimulate plasma cell growth, antibody production and humoral immunity.

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16
Q

What is the main role of CD8+ T cells?

A

Recognise antigens on class I major histocompatibility complexes triggering cell mediated immunity in response to viral infection.

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17
Q

What is the role of the N terminals on an assembled immunoglobulin?

A

Recognition of the antigen

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18
Q

What is the role of the C terminal on an assembled immunoglobulin?

A

Directs antigen to specific receptors to generate response.

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19
Q

What does B lymphocyte antibody release depend on?

A

Cytokine release.

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20
Q

Describe the functions of antibodies.

A

Opsonisation- antigen recognisable to immune cells
Neutralisation- antibodies bind to bacterial toxin
Complement activation- 32 proteins in the blood
Antibody dependent cytotoxicity

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21
Q

What are dendritic cells?

A

First responders to periphery infections, responsible for the uptake of microorganisms for antigen presentation.

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22
Q

What is humoral immunity?

A

Extracellular microbes are eliminated by B cells, secretion of antibodies.

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23
Q

What is cell-mediated immunity?

A

Macrophages activated by T helper cells

T cytotoxic cells mediate the killing of cells and elimination of infection reservoirs.

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24
Q

What is the whooping cough vaccine made from?

A

Killed virulent organisms

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25
Q

What is the rubella vaccine made from?

A

Live non-virulent strains

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26
Q

What is the diphtheria vaccine made from?

A

Chemical/heat treated toxins

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27
Q

What is the influenza vaccine made from?

A

Isolated antigens

28
Q

What is the hepatitis B vaccine made from?

A

Isolated and genetically engineering antigens

29
Q

What is the cholera vaccine made from?

A

Oral vaccine containing dead cells

30
Q

What is the hepatitis A vaccine made from?

A

1) passive immunoglobulin for short term protection

2) inactivated virus in IM injection

31
Q

What are the meningitis vaccines made from?

A

Polysaccharide conjugated vaccines

32
Q

What is the rabies vaccine made from?

A

IM embryonated egg inactivated virus

33
Q

What is the tick borne encephalitis vaccine made from?

A

Inactivated organisms

34
Q

What is the typhoid fever vaccine made from?

A

Capsular polysaccharides

35
Q

What is the yellow fever vaccine made from?

A

Live attenuated viruses

36
Q

What is the varicella vaccine made from?

A

Live attenuated virus that is freeze dried

37
Q

What is the first line of defence in response to viral infection?

A

Increase expression of class I and II glycoproteins to facilitate recognition of viral antigens, activation of NK and macrophage cells, direct inhibition of viral replication

38
Q

What is the second line of defence in response to viral infection?

A

Binding of antibodies, activation of NK and macrophage cells via ADCC, immunoglobulins enhance phagocytosis, agglutinate viral particles and activated complements. IgA blocks fusion of viral envelope, activated complements mediate opsonisation and lysis.

39
Q

What is the third line of defence in response to viral infection?

A

T cell recognition of antigens, Tc cells kill virus infected cells.

40
Q

When is antibody neutralisation of viruses most effective?

A

When a virus is present in large fluid/moist areas

41
Q

Describe cytotoxic T lymphocyte response to viral infection.

A

TCR-MHC mediated recognition of target cell conjugation, re orientation of killing machinery via polarisation. Vesicles containing lytic granules, T cell microtubules, golgi and granules line are oriented towards the target cell. Lytic granules fuse with the membrane, cytotoxins form pores on the target cell, CTL dissociates and the cell dies by apoptosis due to perforin release.

42
Q

What is anaphylaxis?

A

Severe allergic reaction causing respiratory distress and swelling of the larynx often followed by vascular collapse or shock.

43
Q

What is atopy? Why does this occur?

A

Predisposition to development of an allergic reaction due to an overproduction of Th2 cytokines and often exhibit insufficient Th1.

44
Q

When does allergy occur?

A

When the immune system mounts an excessive response to a specific trigger that most people would find innocuous.

45
Q

Which three common allergic disorders predispose to each other?

A

Atopic dermatitis (eczema)
Allergic rhinitis
Asthma

46
Q

What is the most likely cause of drug induced allergy?

A

Biotransformation by hepatocytes, the extent of covalent bonding determines allergy onset. It is dependent on the proportion of a chemical converted into a reactive metabolite.

47
Q

What are the most common food allergies?

A 
Cow's milk
Eggs
Peanuts
Seafood
Soy
Wheat
48
Q

How do symptoms of food allergy develop?

A

IgE synthesis increases and elevation of the number of cytokines produced occurs. IgE mediated reactions occur within minutes to hours however, non IgE mediated reactions can take days to occur

49
Q

What are the common IgE mediated symptoms of food allergy?

A 
Angioedema
Nausea
Hives
Itching
Swelling of the throat
50
Q

What are the physiological effects of histamine 1?

A 
Narrowing airways
Diarrhoea
Pain/itching
Minor increase in HR
Increased mucus production
51
Q

What is the main physiological effect of histamine 12?

A

Gastrin induced acid secretion

52
Q

What are the common side effects of antihistamines?

A

Sedation
Dry mouth
Hypotension
Reflex tachycardia

53
Q

What are glucocorticoids? What is their role in immune response?

A

Steroids produced in the adrenal cortex with 21 carbon atoms. Code for specific cytokines that prevent cell mediated immunity, cause immunosuppression, inhibit T cell proliferation, B cell clonal expansion and antibody synthesis.

54
Q

What is SCID? What is the result?

A

Severe combined immunodeficiency stems from defects in lymphoid development, characterised by low circulating lymphocytes. Failure to mount T cell mediated response, the thymus does not develop and circulating T cells cannot proliferate.

55
Q

What is primary immunodeficiency?

A

Mutations affecting genes that control expression of immune responses. Defect is prevent at birth but may not manifest immediately.

56
Q

What is malignancy?

A

Potential mechanisms cancer cells are able to use to escape immunorecognition.

57
Q

What is first panel malignancy?

A

Tumours can have low immunogenicity lacking recognisable antigens or MHCs express inhibitory molecules to repress T cell function.

58
Q

What is second panel malignancy?

A

Tumour specific antigens cross presented by dendritic cells without co-stimulatory signals, T cell tolerance.

59
Q

What is third panel malignancy?

A

Initially express antigens that the immune system can respond to and eradicate. Genetic instability allows antigenic change as part of an equilibrium phase, where cells lacking immunogenic antigens can expand.

60
Q

What is fourth panel malignancy?

A

Tumours produce growth factors, interleukins, indolamine 2,3-dioxygenase programmed death ligand 1. These can suppress immune responses directly or recruit regulatory T cells.

61
Q

What is fifth panel malignancy?

A

Tumours secrete molecules such as collagen producing physical barriers to prevent lymphocyte access.

62
Q

How do clinically relevant glucocorticoids work? give examples.

A

Immunosuppressants. Inhibit interleukin-1 and TNF gene expression. Decreasing activation of T cells, chemotaxis by neutrophils and release of leukotrienes. Prednisolone, methylprednisolone

63
Q

What is cyclosporin?

A

Immunosuppressant medication that binds to cyclophilins in the cytoplasm which bind to calcineurin resulting in the inability to dephosphorylate NFATc, inhibiting IL-2 production.

64
Q

What is tacrolimus?

A

Suppresses peptide-prolyl isomerase by binding to FKBP-12 and inhibiting calcineurin. Acts as an immunosuppressant.

65
Q

What is sirolimus (rapamycin)?

A

Macrolide antibiotic that binds to FKBP-12 inhibiting a protein kinase, blocking cell cycle S phase.

66
Q

What is mycophenolate mofetil (cellcept)?

A

Cytotoxic drug that is selective for B and T lymphocytes, blocking guanosine nucleotide synthesis.

67
Q

What is muromonab-CD3?

A

A monoclonal antibody that binds to CD3 receptors and inteferes with TCR binding to antigen and inhibits signal transduction resulting in immunosuppression.

Pharm Y2S1 (8 decks)

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