Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

CLS > Immunology - CLS > Flashcards

Immunology - CLS Flashcards

1
Q

Material recognised and damaged in Immunity

A

Both foreign

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Material recognised in allergy/hypersensitivity

A

Foreign recognised, self damaged

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Material recognised/damaged in Autoimmunity

A

Both Self

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Type 1 Hypersensitivty

A
  • Atopic allergy/immediate hypersensitivity
  • Involves allergens, mast cells and IgE
  • Produce high levels IgE, binds to mast cells
    • Recognise antigens of allergen
    • IgE produced against allergen
    • Mast cell degranulates
      • Instant: Histamine, Heparin, tryptase
      • Produces: arachadonic acid-> prostaglandins, leukotrines, cytokines
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Role of Th2 cells in IgE and eosinophil development

A
  1. Alleregen taken up by APC
  2. Peptide loaded to HLA II
  3. Interacts with CD4 of TH2
  4. TH2 produces cytokines
  • IL-4 causes calss switching to IgE specific to allergen
  • IL-5 stimulates eosinophils; degranulate, tissue damage, hypersensitivity
  • IL-10 co-stimulates mast-cell growth; more deranulation etc
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Different routes of allergen entry and their response

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Outline Skin prick test

A

Inject 0.02ml of an extract of particular antigen

  • immediate reaction: 20 min, IgE activated
  • immediate+late: IgE +/- Tcells activated
  • delayed: TH1 cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Outline type II hypersensitivity

A

antibodies produced by immune system bind to own antigen on own cells

e.g. haemolytic disease of newborn

Blood transfusions

Goodpasture’s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Outline type III hypersensitivity

A
  1. Immune complexes too large
  2. Not enough complement/RBS to clear antigen
  3. Immune complexes deposited in tissues
  4. Antibodies bind to neutrophils; tissue damage

e.g. Extrinsic allergic alveolitis (allergy)

  • ABs to fungal spores; repeated exposure cause increased size of complexes
  • Complexes deposit in lungs
  • Fc interaction with neutrophils; relase mediators; tissue damage i.ie farmers lung

Autoimmune e.g.g SLE, rheumatoid arthritis

(An immune complex, sometimes called an antigen-antibody complex, is a molecule formed from the integral binding of an antibody to a soluble antigen.[1] The bound antigen and antibody act as a unitary object, effectively an antigen of its own with a specific epitope. After an antigen-antibody reaction, the immune complexes can be subject to any of a number of responses, including complement deposition, opsonization,[2] phagocytosis, or processing by proteases. Red blood cells carrying CR1-receptors on their surface may bind C3b-coated immune complexes and transport them to phagocytes, mostly in liver and spleen, and return to the general circulation.)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Outline type IV hypersensitivity

A
  • Not anti-body mediated, cell-mediated (T cell)
  • Chronic overstimualtion of macrophages by excessive cytokine release
  • Macrophages form multinucleated giant granulomas; tissue damge
  • e.g. Contact dermatitis (allergy), pulmonary TB, LEprosy
  • e.g. Autoimmune Thyroiditis, addisons, gastritis, T1DM
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Immunological basis of tissue transplant rejection

A

Recipient and donor not genetically identical, different range of HLA alleles

Leads to type IV Hypersensitivity

  1. APC donor cells in allograft present foreign antigens to recipient TH(due to need for protein binding for stability)
  2. Recognised as being different to recipeint’s HLA
  3. Trigger TC and macrophages
  4. Donor cells destroyed

Treat by lifelong immunosupressants

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Antigen recognised in SLE

A

Double stranded native DNA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Antigen recognised in rheumatoid arthtritis

A

Synovial IgG

/Rheumatoid factor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Outline Autoimmune aspect of Grave’s disease

A

TSHR stimulating antibodies

  1. Stimulates thyroid hormone production
  2. Not regulated anymore by feedback;overproduction = hyperthyroidsism

Anti-TSHR can pass to foetus; neotal graves

Features of graves:

  • Diffuse goitre, weight loss, irratable
  • Graves Ophtalmopathy
    • Inflammation of extra-occular tissues
    • Pushes eyes forwards
  • Pretibial myxodeama
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Outline immuno basis of atrophic thyroiditis

A

Hypothyroidism (type IV)

Caused by TSHR _blocking(_not stim) antibodies

  • Block TSH bidnning; destruction and fibrosis of thyroid tissue
  • Atrophy; hypothyroidism

Weight gain, depression, primary myxodeama

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Outline Immuno of Hashimoto’s thyroidits

A

Antibodies to thyroid peroxidase & thyroglobulin

  • Leads to destruction of thyroid tissue
  • Hypothyrodisism
  • Goitre(due to infiltration of lymphocytes rather than proliferating thyroid celles in graves)
17
Q

Autoimmune basis of pernicious anaemia

A

TYPE IV

  • Autoimmune destruction of gastric parietal cells
    • reduces IF production: less B12 absorbed
  • Production of AB to intrisic factor; bind; block or decrease IF/B12 interaction.
  • Less B12 absorbed from gut, affect proliferating cells e.g. reticulocytes
  • Tired, washed out. treat by b12 injections
18
Q

Outline autoimmune basis of T1DM

A

Caused by autoreactive T cells

Destroys insulin-producing beta-cells

19
Q

Immunological basis of Mysthenia gravis

A

Type II

cause: Autoantibodies specific for ACh receptors

  1. inhibits ACh receptors; block binding
  2. Induce receptor internalisation and degradation
  3. Lack of nerve stimulus of muscle contraction

Treat by anticholinesterase; blocks breakdwon of ACh

20
Q

Autoimmune haemolytic anaemia

A

TYPE II

cause: Autoantibodies specific for RBC surface antigen

  • Opsonisation of RBS, inducing
    • Complement activaition; lysis, RBC destruction
    • Desctruction by phagocytes
21
Q

Goodpastures disease

A

TYPE II

Cause: autoantibodies specific for type IV collagen

  • Binds directly to glomerular basement membrane
  • Activatin of complement and neutrophils
  • Tissue damage, kidney failure
  • Also bind to BM of alveoli; lung damage
22
Q

Pemphigus vulgaris

A

TYPE II

Cause: Autoantibodies to epidermal cadherin

  • Blisters
23
Q

SLE

A

Type III/II

cause: Autoantibodies to a range of ubiquitous cellular constituents

  • Complexes forms, deposit in various tissues; damages
    • Glomeruli, nephritis
    • Skin, joints, sCNS
    • Buttefly rash
24
Q

Rheumatoid arthritis

A

cause: Rheumatoid factors specific for IgG

  1. Bind and form complexes
  2. Targets synovial joints
25
Q

Primary vs Secondary immunodfeiciency

A

10: Inherited

Mainly autosomal recessive, some X-linked

20: Acquired (manifest in adults)

From enviornment or other disease processes

26
Q

Characteristics of infections in immunodeficient patient

A

Serious

Persistent

Unusual

Recurrent

27
Q

Antibody deficiencies

A

Commonly have

  • bacterial infection (ears, sinus, chest)
  • giardi gut infection
  • Permanent damage

Other

  • Enteroviral infection
28
Q

Examples of antibody deficiencies

A

Bruton’s disease: X-linked

  • presents early
  • encodes tyrosine kinase essential for B cell development from precursors; no ABs in blood

Hyper IgM syndrome:

  • Defective Th, don’r activate B cells or cause class shifting
  • Unusally high levels of IgM
29
Q

Primary T cell deficiency

A

E.g. DiGeorge syndrome

  • Thymus (reduced/absent)
    • Infections: fungal, viral
30
Q

AIDS as a secondary T cell deficiency

A

Caused by HIV infection

  • Binds to CD4
    • Infects Th
    • Tc kill infected Th
    • Progressive decline in CD4 cells
    • Worsening immune function

Appearance of opportunistic infections: Karposis, Pneumonia, cryptosporidum

31
Q

Outline SCID

A

Primary immunodeficiency from inherited stem cell defect; lack of functional lymphocytes

  • Increased susceptibility to all infectious agents

Bone marrow transplantation

32
Q

Neutrophil deficiencies

A

Reduced numbers

  • Primary: Kostmanns, cyclic neutropenia
  • Secondary: Leukaemia, chemotherapy, infection

Abnormal function

  • adhesion deficiency
  • chemotaxis
  • killing activity by defects in enzymes; increased bacterial and fungal infections
33
Q

Complement deficiencies

A

Particularly associated with bacterial infections

34
Q

Main categoriesof secondary immunodeficiencies

A

Latrogenic

  • Immunosupressive treatment

Malignancies of immune system

  • Leukaemia, Lymphoma, Myeloma

Inections

  • HIV, malaria, measles

Malnutrition

35
Q
A

CLS (20 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions