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MRCS > Immunology > Flashcards

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

A

Class 1

24
Q

Which MHC class presents exogenous antigens to signal CD4 T cells

A

Class 2

25
Q

HLA associated diseases :
B27
DR 2
DR 3
DR4

A

HLA B27= ankylosing spondylitis/ reiters disease

HLA DR2= Good pastures

HLA DR3= Hashimotos, Addisons, Myaesthenia gravis

HLA DR4= T1DM

26
Q

Where do all lymphoid tissue originate from pleuripotent cells

A

Bone marrow

27
Q

WHere do cells that are destined to become T and B cells go?

A

T cells- Thymus
B cells- stay in bone marrow

28
Q

What are the primary and secondary lymphoid organs

A

Primary= Thymus + Bone marrow
Secondary= Lymph nodes, spleen, Mucosa Associated Lymphoid tissue (MALT)

29
Q

What are the 2 complement pathways

A
30
Q

What are the functions of different complements (C3a, C4a, C5a, C3b, C5-9)

A
31
Q

What are the types of hypersensitivity reactions

A

Type 1,2,3,4,5 (ACIDS)

32
Q

What is Type 1 hypersensitivity and what are the factors involved

A

Type 1- allergy/ anaphylaxis

IgE antibodies bound to allergens/ antigens cause mast cells/ basophils to release mediators that give the symptoms of allergy

33
Q

What is Type 2 hypersensitivity and what are the factors involved

A

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
Q

What is Type 3 hypersensitivity and what are the factors involved

A

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
Q

What is Type 4 hypersensitivity and what are the factors involved

A

Type 4= Delayed hypersensitivity

T-cells involved

Takes 2-3 days to develop

eg: Tuberculin test, allergy tests, dermatitis, tissue/ organ transplant rejection

36
Q

What is Type 5 hypersensitivity and what are the factors involved

A

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
Q

Examples of phagocytic cells

A

neutrophils, monocytes, macrophages, kuppfer cells

38
Q

Eg of infective causes of Type 3/ immune complex disease

A

post-strep glomerulonephritis
Hep B/C
CMV
Malaria

39
Q

What antibodies/ antigens (A/B) does someone with a blood group O have

A

AB antibodies (can only receive from O)

No antigens (universal donor)

40
Q

What antibodies/ antigens (A/B) does someone with a blood group AB have

A

No Antibodies (universal recipient)

AB antigens

41
Q

What antibodies/ antigens (A/B) does someone with a blood group A have

A

Group A:
Antibodies-B
Antigens- A

Group B:
Antibodies-A
Antigens-B

42
Q

What are Kinins and some of their functions

A

Kinins are polypepides/ proteins/ enzymes

Vasodilation
increased vascular permeability
attract phagocytes

43
Q

Which conditions show a high titre of:
-ANCA
-pANCA
-AMA
-anti-SMA + ANA + dsDNA
-anti-EMA + ttG
-anti-CCP
-anti-Scl70

A

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
Q

What are the effects of Thromboxane

A

vasoconstriction
increased vascular permeability
aggregation of platelets

45
Q

Timeframes and management of
hyperacute rejection
acute rejection

A

Hyper acute= mins-hrs [remove donor organ]

accelerated acute= 2-4 days

acute= 1week- 3months [corticosteroids]

chronic= months-years [ciclosporin/ steroids]

46
Q

Cause and management of hereditary angio-oedema

A

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
Q

What cells produce leukotrienes and what are the actions of leukotrienes

A

Mast cells

Leukotrienes cause:
vasoconstriction
bronchoconstriction

48
Q

MOA of ciclosporin in immunosuppression

A
49
Q

What do the following hepatitis antigens/ antibodies indicate

anti-HBs
anti-HBc
anti-HBe
HBsAg
HBcAg
HBeAg
IgG HBcAg
IgM HBcAg

A

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
Q

What are the mediators in the 2 phases of type 1 hypersensitivity response

A

Early phase:
-histamine
-prostaglandin D2
-leukotrienes C4, D4
-serotonin
-proteases

late phase:
prostaglandins
leukotrienes
bradykinin

51
Q

What produces the mediators in the early and plate phases of a type 1 hypersensitivity reaction

A

early= mast cells

late= mediators are products of metabolism of arachadonic acid

52
Q

Why should hydrocortisone be given following anaphylaxis

A

to prevent the late phase of type 1 hypersensitivity rxn

(prevents formation of prostaglandins and leukotrienes)

MRCS (22 decks)

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