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X. MRCS: Physiology > Immunology > Flashcards

Immunology Flashcards

1
Q

Types of immune response

A

Innate

Adaptive

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2
Q

Features of innate immune system

A

Immediate
Non-specific
Lacks memory

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3
Q

Features of the adaptive immune system

A

Takes few days to start, peaks at 1-2 weeks
Highly specific
Has memory

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4
Q

Components of the innate immune system

A

Barriers
Cytokines
Cells (from common myeloid progenitor)
Compliment

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5
Q

Common myeloid progenitor cells

A 
Generates:
Megakaryocyte (then makes platelets)
Erythrocyte (RBCs)
Mast cells
Myeloblast
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6
Q

Myeloblast

A

Resides in bone marrow. Activated by cytokines.
Generates:
Basophil
Neutrophil
Eosinophil
Monocytes (creates macrophage and dendritic cells)

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7
Q

Common lymphoid progenitor

A

Generates:
Natural killer cells
Small lymphocytes (then matures to T lymphocytes and B lymphocytes)

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8
Q

Neutrophils

A

Innate immune system. First cells to arrive at site of infection.
Granular leukocyte. Multi-lobed nucleus.
Most abundant WBC (40-70% of plasma)
Main action against bacteria/fungal.
Phagocytose mircoorganisms.

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9
Q

Monocytes

A

Involved in response to bacteria infection.
Kidney bean shaped nucleus.
5-10% of plasma WBCs
Remain in blood before migrating into tissues and differentiating into macrophage.

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10
Q

Macrophage

A

Main population of phagocytic cells within tissues. Longer lifespans (months-years).
Large, single-lobbed, round nucleus.
Phagocytose microorganisms

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11
Q

Organ/tissue specific macrophages

A

CNS - microglial cells
Liver - Kupffer cells
Lungs - Alveolar macrophages
Skin/mucosa - Langerhans cells

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12
Q

Dendritic cells

A

Antigen presenting cells.
Linking innate and adaptive immune systems.
Activate naive T cells by presenting antigens on MHC II.

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13
Q

Eosinophils

A

1-3% of circulating WBCs
Bi-lobed, sausage shaped nucleus.
Granules contain (Major basic protein, cationic protein, peroxidase), molecules toxic to parasites.
Main action is against parasitic infections.
Phagocytose antigen-antibody complexes.
Also increased in allergy/autoimmune disease

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14
Q

Basophils

A

Bi-lobed S shaped nucleus
Contain histamine granules.
Cause local inflammatory response through interaction with IgE.
Mediate type 1 hypersensitivity reactions

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15
Q

Lymphocytes

A

Agranular WBCs.
Respond to viral infection
Round densely-staining nuclei.
Differentiate to: NK cells, T cells, B cells

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16
Q

Natural killer cells

A

Non-specific immunity against cells displaying foreign proteins (cancer/virally infected cells).
Detect and kill pathogens as part of innate.
Detect abnormal cells and release perforins and cytolytic proteins causing lysis.

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17
Q

T cells

A

Form in bone marrow, mature in thymus.
Adaptive immune system.
Types: cytotoxic (CD8), T-helper (CD4), Memory T.

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18
Q

Cytotoxic T cells

A

CD8
Activated by MHCI (on infected normal cell)
Stimulated by IL-12/IL-18.
Kill virus infected cells

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19
Q

T-helper cell

A

CD4
Activated by by MHCII (antigens presenting cell)
Many different types

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20
Q

B cells

A

Form and mature in bone marrow
Adaptive immune system
Humeral immunity by secreting antibodies
Mature into plasma cells (antibody secreting cells) and B memory cells

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21
Q

Cytokines - functions

A

Pro-inflammatory

Homeostatic

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22
Q

Cytokines: pro-inflammatory functions

A

Chemokine: recruit immune cells to site of infection/injury

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23
Q

Cytokines: homeostatic functions

A

Attracting cells acquired for angiogenesis
Immune surveillance and allowing T-cell/dendritic cells to migrate
Development of lymph organs

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24
Q

Types of cytokines

A

Interferons
Interleukins
Tumour necrosis factor

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25
Q

Interferons

A

Released by host cells in response to pathogen and tumour cells
Type-I (interferon-alpha/beta)
Type-II (interferon-gamma)
Type-III

26
Q

Type-I interferons (interferon alpha/beta)

A

Interfere with viral replication
Autocrine/paracrine signalling
Up regulate NK cells and MHCI on surface (meaning NK and cytotoxic T can more easily recognise infected cell)

27
Q

Type-II interferons (interferon-gamma)

A

NK, cytotoxic T and Th1 all produce interferon gamma in response to IL12/IL18
Activates macrophages and increases ability to kills pathogens by enhancing pinocytosis and lysosome function
Upregulates MHCII expression

28
Q

Interleukins

A

Produced by T cells, monocytes and macrophages
Promotes production and differentiation of B and T lymphocytes
Activates neutrophils and NK
Produces fever (IL-6), raises acute phase proteins (CRP)
Promotes vascular permeability, increasing recruitment of cells to area of infection/injury

29
Q

Tumour necrosis factor

A

Produced by macrophages when encountering endotoxin
Can be produced by mass cells/B cells/T cells
TNF alpha/beta:
Local induction of apoptosis
Increasing vascular permeability
Neutrophil chemotaxis
Suppression of appetite

30
Q

Complement

A

Part of innate immunity

Complement components mostly made in liver.

31
Q

Complement system: activation

A

Classical pathway
Mannose-Binding Lectin pathway
Alternative pathway
All 3 pathways produce C3 convertase

32
Q

Complement system: effects

A

C3 convertase - activates C5, which activates C6, C7, C8, C9 in a cascade.
Opsonisation (C3b binds to antigens on pathogen stimulating neutrophils/macrophases to phagocytose)
Lysis of pathogens (membrane attack complexes, formed from C5b + several factors. MAC ruptures bacterial cell membrane)
Chemotaxis (attracts neutrophils/macrophages to site of infection)
Inflammation (C3a/C4a/C5a bind to mast cells/basophils and cause degranulation. Histamine and serotonin release increases vascular permeability)

33
Q

Barriers to infection

A

Physical
Physiological
Chemical
Biological

34
Q

Barrier to infection: physical

A

Skin: multiple layers of dead, keratinised epithelium
Mucous membranes: resp/GI/urinary. Epithelial layer has tight junctions.
Bronchial cilia.
Secretion: tears, urine, saliva, bila, mucus

35
Q

Barriers to infection: physiological

A

Diarrhoea
Vomiting
Coughing
Sneezing

36
Q

Barriers to infection: chemical

A

pH: skin (5.5), gastric (1-3), vagina (4.4)
Molecules:
IgA (tears/saliva/mucous membranes)
Lysozyme (sebum, sweat, panted cells in small bowel)
Mucus
Defensins
Enzymes

37
Q

Barriers to infection: Biological barriers

A

Normal flora are non-invasive commensal microorganisms.

Outcompete pathogens for attachments and resources

38
Q

Components of the adaptive immune system

A

Antibodies

Cells (NK, cytotoxic T, Th, B)

39
Q

Antibodies: structure

A

2 heavy chains

2 light chains

40
Q

Antibodies: classification/types

A 
IgG
IgA
IgM
IgD
IgE
41
Q

IgG

A

Most abundant
Present on surface of mature B cells
Only antibody able to cross placenta

42
Q

IgA

A

Move prevalent antibody in secretions, forms a barrier layer at mucosal surfaces
High levels in breast milk
Neutralises pathogens and hinders attachment to epithelial receptors

43
Q

IgM

A

Expressed on surface of B-cells an monomers
Secreted as pentameters
First to be produced during foetal development
First to be produced by B-cells against new infection.

44
Q

IgD

A

Present of surface of B cells.

Has role in B cell and antibody production

45
Q

IgE

A

Mainly found on mast cells
Associated with allergy, and type 1 hypersensitivity reactions
Triggers histamine release from mast cells and basophils
Part of response to parasitic infections

46
Q

Functions of antibodies

A 
Opsonisation
Neutralisation
Complement activation
Immune complexes
Antibody mediated cell mediated cytotoxicity
47
Q

Antigen presentation

A

Major histocompatibility complexes (MHC)
MHC I: all nucleated cells
MHC II: antigen presenting cells

48
Q

Antigen presenting cells

A

MHC II
Dendritic cells
B cells
Macrophages

49
Q

T cells and antigen presentation

A

T cells recognise MHCs using T-cell receptor (TCR)
Coreceptors:
CD4 (Th): MHC II
CD8 (Cytotoxic): MHC I

50
Q

Hypersensitivity reactions

A

Type I
Type II
Type III
Type IV

51
Q

Type I hypersensitivity

A

Allergic/anaphylactic

IgE mediated

52
Q

Type I hypersensitivity: pathophysiology

A

First exposure: APCs present antigen to naive T-cells, turning them into Th2. IL4/IL5/IL10 release. IL4 causes B cells to produce specific IgE. IL5: eosinophils. IgE binds to mast cell surface.
Second exposure: mast cells with specific IgE degranulate (histamine, proteases)

Early phase (minutes): H1 receptor (bronchial smooth muscle contraction, blood vessel dilation/inc permeability

Late phase (8-12hs): eosinophils/basophils/Th2 mediated by IL4/IL5/IL10

53
Q

Type 1 hypersensitivity: examples

A

Atopic disease
Asthma
Anaphylaxis
Churg-Strauss Syndrome

54
Q

Type 2 hypersensitivity

A

“Cytotoxic” or Antibody dependent

IgM/IgG/complement/MAC mediated

55
Q

Type 2 hypersensitivity: pathophysiology

A

Self-reactive B cells are not destroyed and form a IgM or IgG (assisted by CD4 cells)
These antibodies bind to antigens on the surface of host cells: Intrinsic antigens (normally made by host cells) or Extrinsic antigens (attaches to the host cell)
5 mechanisms:
1: complement activation (C3a/C4a/C5a) & neutrophil degranulation
2: MAC
3: Opsonisation and phagocytosis
4: antibody dependent cell mediated cytotoxicity (ADCC): NK degranulation
5: antibody mediated cell dysfunction (non-cytotoxic, e.g. myasthenia graves/graves)

56
Q

Type 2 hypersensitivity: examples

A 
Autoimmune haemolytic anaemia
Rheumatic heart disease
Goodpasture's syndrome
Grave's disease
Myasthenia gravis
57
Q

Type 3 hypersensitivity

A

Immune complex mediated

IgG, complement and neutrophil

58
Q

Type 3 hypersensitivity: pathophysiology

A

IgG binds to soluble antigen forming immune complex
Deposits in basement membrane of vessels and causes compliment activation
Neutrophils attempt to phagocytose but cannot and degranulate into vessels, causing vasculitis
Disease where immune complexes are deposited (kidneys/joints)

59
Q

Type 3 hypersensitivity: examples

A

Systemic lupus erythematosus
Serum sickness
Rheumatoid arthritis
Post-strep glomerulonephritis

60
Q

Type 4 hypersensitivity

A

Cell-mediated immune response

T cell

61
Q

Type 4 hypersensitivity: pathophysiology

A

APC presents antigen using MHCII to Th
Th matures to Th1 (effector cell)
Th1 produces IL12, IFN-gamma (activates macrophages). Activated macrophages release pro-inflammatory cytokines and lysosomal enzymes/complement/ROS (causing tissue damage)

62
Q

Type 4 hypersensitivity: examples

A 
Contact dermatitis
Graft versus Host disease
Multiple sclerosis
Coeliac disease
Hashimoto's thyroiditis

X. MRCS: Physiology (4 decks)

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