Immunology Flashcards

1
Q

What are the 2 types of immunity

A

innate (non-specific)

adaptive (specific)

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2
Q

What are the components of innate immunity

A

-physical barriers (skin)
-mechanical factors (cough/ cilia)
-secretions (tears/ saliva)
-cellular factors (phagocytic/ NK cells)

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3
Q

What are the 2 types of acquired immunity

A

Cell mediated- T cells

Humoral -B cells/ antibodies

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4
Q

What is an antigen

A

Anything that brings about an immune response

and

anything that binds specifically to antibodies/ T-cell antigen recpetors.

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5
Q

What are the actions brought about by antibodies binding to antigens

A

-lysis of bacteria
-neutralization of toxins
-opsonization (mark antigen for other cells to come and destroy)
-antibody dependent cell mediated cytotoxicity

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6
Q

What cells produce antibodies

A

B cells that differentiate into plasma cells

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7
Q

Where are antibodies produced

A

lymph nodes
spleen
bone marrow

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8
Q

What are the 5 different classes of immunoglobulins

A

IgG
IgA
IgM
IgE
IgD

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9
Q

Which is the heaviest Ig/ has the most antibody binding sites

A

IgM

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10
Q

Which Ig is the most abundant in the plasma AND can cross the placenta

A

IgG

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11
Q

Which Ig are characteristic of the
primary immune response
secondary immune response

A

primary= IgM
secondary= IgG

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12
Q

Which Ig is responsible for protection of mucosal surfaces and how

A

IgA

production of secretions- tears, saliva, sweat, mucus
present in respiratory and GI tract

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13
Q

What are the functions of IgE

A

anaphylactic reactions
anti-parasitic

stimulates mast cells, basophils and recruits eosinophils

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14
Q

Which Ig cause complement activation

A

IgG IgM

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15
Q

Functions of IgD

A

help in B cell differentiation
acts as a lymphocytic membrane receptor

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16
Q

Functions of IgG

A

Neutralises toxins
opsonizes bacteria
characteristic of secondary immune response

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17
Q

Functions of IgM

A

opsonizes and agglutinates bacteria
characteristic of primary immune response

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18
Q

What cells are responsible for cell-mediated immunity

A

T cells

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19
Q

What are the different types of T-cells

A

CD4- T helper
CD8- cytotoxic T cells
CD25- activated cytotoxic T cells

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20
Q

What is the function of T-helper cells

A

present antigens and activates CD8, B cells and macrophages

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21
Q

Once activated what do cytotoxic T cells do?

A

destroy infected target cells

22
Q

What is MHC and what is their role in the immune response

A

Major histrocompatibility complex- are genes that code for glycoproteins on membrane surfaces

they present antigens to T cells

23
Q

Which MHC class presents endogenous/ viral antigens to signal CD8 T cells

24
Q

Which MHC class presents exogenous antigens to signal CD4 T cells

25
HLA associated diseases : B27 DR 2 DR 3 DR4
HLA B27= ankylosing spondylitis/ reiters disease HLA DR2= Good pastures HLA DR3= Hashimotos, Addisons, Myaesthenia gravis HLA DR4= T1DM
26
Where do all lymphoid tissue originate from pleuripotent cells
Bone marrow
27
WHere do cells that are destined to become T and B cells go?
T cells- Thymus B cells- stay in bone marrow
28
What are the primary and secondary lymphoid organs
Primary= Thymus + Bone marrow Secondary= Lymph nodes, spleen, Mucosa Associated Lymphoid tissue (MALT)
29
What are the 2 complement pathways
30
What are the functions of different complements (C3a, C4a, C5a, C3b, C5-9)
31
What are the types of hypersensitivity reactions
Type 1,2,3,4,5 (ACIDS)
32
What is Type 1 hypersensitivity and what are the factors involved
Type 1- allergy/ anaphylaxis IgE antibodies bound to allergens/ antigens cause mast cells/ basophils to release mediators that give the symptoms of allergy
33
What is Type 2 hypersensitivity and what are the factors involved
Type 2= cytotoxic cell mediated IgG and IgM involved Circulating antibodies interact with antigens on cell surfaces to cause cell death eg: rhesus incompatibility, haemolytic anaemia, ITP, transfusion reactions
34
What is Type 3 hypersensitivity and what are the factors involved
Type3= Immune complex mediated IgG and IgM involved Antibody-antigen form complexes and cause inflammatory reactions where they land and activate COMPLEMENT cascades causing tissue destruction eg: SLE, RA, serum sickness, post-strep glumerulonephritis
35
What is Type 4 hypersensitivity and what are the factors involved
Type 4= Delayed hypersensitivity T-cells involved Takes 2-3 days to develop eg: Tuberculin test, allergy tests, dermatitis, tissue/ organ transplant rejection
36
What is Type 5 hypersensitivity and what are the factors involved
Type 5= Stimulating reactions Antibodies stimulate the receptors against which they act eg: myaesthenia gravis/ graves (TSH receptor antibodies cause prolonged secretion of thyroid hormones)
37
Examples of phagocytic cells
neutrophils, monocytes, macrophages, kuppfer cells
38
Eg of infective causes of Type 3/ immune complex disease
post-strep glomerulonephritis Hep B/C CMV Malaria
39
What antibodies/ antigens (A/B) does someone with a blood group O have
AB antibodies (can only receive from O) No antigens (universal donor)
40
What antibodies/ antigens (A/B) does someone with a blood group AB have
No Antibodies (universal recipient) AB antigens
41
What antibodies/ antigens (A/B) does someone with a blood group A have
Group A: Antibodies-B Antigens- A Group B: Antibodies-A Antigens-B
42
What are Kinins and some of their functions
Kinins are polypepides/ proteins/ enzymes Vasodilation increased vascular permeability attract phagocytes
43
Which conditions show a high titre of: -ANCA -pANCA -AMA -anti-SMA + ANA + dsDNA -anti-EMA + ttG -anti-CCP -anti-Scl70
ANCA= vasculitis/ polyangitis/ UC pANCA= PSC AMA= PBC anti-SMA/ ANA/ dsDNA= SLE/ autoimmune hepatitis anti-EMA/ ttG= coeliacs anti-CCP= RA anti-SCL70- systemic scelroderma
44
What are the effects of Thromboxane
vasoconstriction increased vascular permeability aggregation of platelets
45
Timeframes and management of hyperacute rejection acute rejection
Hyper acute= mins-hrs [remove donor organ] accelerated acute= 2-4 days acute= 1week- 3months [corticosteroids] chronic= months-years [ciclosporin/ steroids]
46
Cause and management of hereditary angio-oedema
Caused due to SERPING1 gene mutation causes reduced levels/ reduced function of C1 esterase inhibitor causes increased levels of bradykinin causes inflammation and increased vascular permeability= oedema
47
What cells produce leukotrienes and what are the actions of leukotrienes
Mast cells Leukotrienes cause: vasoconstriction bronchoconstriction
48
MOA of ciclosporin in immunosuppression
49
What do the following hepatitis antigens/ antibodies indicate anti-HBs anti-HBc anti-HBe HBsAg HBcAg HBeAg IgG HBcAg IgM HBcAg
anti-HBs (surface)- immunity due to vaccine/ recovery from prev infection anti-HBc (core)- prev/ current infection anti-HBe (envelope)- persistent=chronic infection/ less infective HBsAg- acute infection HBcAg- acute infection HBeAg- highly infective IgG HBcAg- pev infection (G=gone) IgM HBcAg- acute infection (M= mantenaint)
50
What are the mediators in the 2 phases of type 1 hypersensitivity response
Early phase: -histamine -prostaglandin D2 -leukotrienes C4, D4 -serotonin -proteases late phase: prostaglandins leukotrienes bradykinin
51
What produces the mediators in the early and plate phases of a type 1 hypersensitivity reaction
early= mast cells late= mediators are products of metabolism of arachadonic acid
52
Why should hydrocortisone be given following anaphylaxis
to prevent the late phase of type 1 hypersensitivity rxn (prevents formation of prostaglandins and leukotrienes)