L20: Hypersensitivity Flashcards

1
Q

what are hypersensitivity diseases

A

diseases caused by the immune response

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

when responses are not adequately controlled or
targeting to ____ then the immune response
becomes ____

A

the wrong tissue, the cause of the disease

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

Type 1 mediated

A

IgE - allergy

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

Type II mediated

A

IgG - antibody mediated (cytotoxic)

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

Type III mediated

A

IgG - immune complex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Type IV mediated

A

TH cells

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

Why do we have IgE responses?

A

crucial in defence against parasite infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Why IgE and not IgG/FcR mediated for T1HS

A
  • Normal IgG/FcR-mediated activity not very effective in mobilising fast response
  • The mast cell receptor affinity for IgE is high and the IgE/FcR response is immediate in the presence of pathogen
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the action of IgE

A

causes mast cell degranulation by binding to FcER receptor and antigen crosslinking IgE

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

what happens when mast cells degranulate?

A

release of mediators
1. chemoattractants
2. activators (blood flow/dilation)
3. spasmogens (smooth muscle contraction, mucous secretions)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Mast cell mediators that are synthesised after activation

A

lipid mediatiors, cytokines

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

mast cell mediators pre-formed, what does this mean?

A
  • biogenic amines (histamines), enzymes (tryptases)
  • immediate release upon activation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

action of histamines

A

vasodilation and vascular leak

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

action of enzymes

A

tissue damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

action of lipid mediators

A

bronchoconstriction, intestinal hypermotility, inflammation

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

action of cytokines

A

inflammation

17
Q

common causes of allergies

A

rhinitis (hay fever), insect stings, food allergies, small molecules (morphine)

18
Q

What is mast cell sensitization

A

The binding of IgE to its high-affinity IgE receptor on mast cell surfaces upon first exposure to allergen

19
Q

What happens upon re-exposure when a mast cell has been sensitized?

A

mast cell preloaded with IgE - triggering a HS reaction

20
Q

allergies treatment

A
  1. avoidance
  2. antihistamines (bind histamine receptor so histamine cant trigger symptoms)
  3. coritcosteroids
  4. epinephrine
  5. desensitisation (gradually increasing dose of allergen to insude high affinity IgG - competes with IgE = stops allergic reaction)
21
Q

allergy testing

A

immunoassay (test for AB to allergen), skin prick

22
Q

Explain the hygiene hypothesis in terms of T helper cells

A

Immune response to common allergens get polarised away from having a Treg/Th1 response to a Th2 IgE response

23
Q

Explain what happens in T2 HS

A
  • Antibodies (IgG/IgM) bind directly to antigens on the surface of cells and cause lysis
  • can attack mobile cells (in blood stream), or antibodies bind fixed/solid tissue
24
Q

what is hemolytic anemia

A

Individual makes
antibodies to their own red
blood cells (RBC)

25
Q

Explain how hemolytic anemia occurs

A
  • IgG coated RBC are cleared from circulation via uptake by Fc receptor bearing macrophages
  • IgM coated RBC are fixed by complement and directly lysed (MAC complex formation)
26
Q

What happens when AB bind to self antigen on tissue (T2 HS)

A
  1. ADCC - antibody dependent cellular cytotoxicity
  2. complement activation
  3. frustrated phagocytosis
27
Q

what is an example of Anti-tissue antibodies

A

goodpastueres syndrome

28
Q

explain how goodpastures syndrome occurs

A
  • Antibodies against type IV collagen in glomerular basement membrane
  • Affects the kidney glomeruli and the alveoli in the lungs
  • Antibodies trigger complement activation that damages epithelial cells
  • Patients present with transient kidney dysfunction and bleeding in the lungs
29
Q

explain what happenscin T III HS

A
  • Antibody complex is not cleared
  • Complex becomes large, insoluble
  • Complexes lodge in sites and provoke an immune response
30
Q

give examples of T III HS

A

serum sickness, rheumatoid arthritis

31
Q

What is Txpe IV HS

A

delayed-type hypersensitvity

32
Q

Type IV HS is mediated by?

A

antigen specific T-cells

33
Q

Explain how TIV HS is established

A

Antigen injected, process by local APC, Th1 effector response, recruitment of phagocytes, inflammation at site

34
Q

What are examples of T IV HS

A

contact sensitivity eg jewellery

35
Q

explain the process of contact sensitivity

A
  • normal proteins act as carrier for small molecule
  • transport to lymph