Brainscape's Knowledge GenomeTM

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


See full index

Immunology > Hypersensitivity Reactions > Flashcards

Hypersensitivity Reactions Flashcards

1
Q

What are some diseases as a result of hypersensitivity reactions

A

Goodpastures, haemolytic, sle, myasthenia Gravos, RA, graves

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

What is hypersnsitivity

A

The term hypersensitivity describes “the antigen- specific immune responses that are either inappropriate or excessive and result in harm to host”
The mechanisms underlying these aberrant immune responses are those employed by the host to fight infections

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

What are types of triggers (antigens

A

• Hypersensitivity to exogenous antigens  Non infectious substances (innocuous)
 Infectious microbes
 Drugs (Penicillin)
• Hypersensitivity to intrinsic antigens  Infectious microbes (mimicry)
 Self antigens (auto-immunity)

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

What are teh types of hypersensitivity reaction

A

• Type I or immediate (Allergy) - IgG
• Environmental non infectious antigens
• Type II or antiBody mediated -IgG, IgM - antigen on cell/tissue
• Type III or immune Complexes mediated- igG, IGM - soluble antigen
• Type IV or cell mediated (Delayed)
 Environmental infectious agents and self antigens
- aleren, rest, self antigen

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

Whar are common features of hypersensitivity reaction

A

• Sensitization phase
 First encounter with the antigen. Activation of APCs and memory effector cells. A previously exposed individual to the antigen is said to be “sensitized”
• Effector phase
 Pathologic reaction upon re-exposure to the same antigen and activation of the memory cells of the adaptive immunity
First - o clinical manifestation. Second encounter - clinical manifestation.

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

Describe type 2 hypersensitivity

A 
• Usually develops within 5-12 hr
• Involves IgG or IgM antibodies
• Targets cell bound antigens
- Exogenous: Blood group antigens, Rhesus D antigens
- Endogenous: self antigens
• Induces different outcomes
-  Tissue/cell damage
-Physiological change
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Describe type 2 hypersensitive machanisms

A

Cell expressing self antige - person expose to trigger - mounted immune resopns - secon eounter - antibody binds to self antigen - 2 things happen: (complement activation, antibody dependent cell cytotoxicity)
Immune mechanisms. Once compliment ctivated then (Complement activation
 Cell lysis (MAC)
 Neutrophil recruitment/
activation (C3a/C5a)  Opsonisation (C3b)) compliment also releases neutrophil - damage cell/tissue. Opsonised - eutrophi then engulfs cel. FC receptors

Antibody-dependent cell cytotoxicity
(NK cells)

Receptor stimulation

Receptor blockade

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

What are examples of type 2 hypersensitivity

A 
Haemolytic disease of the
newborn (HDN)
- Antigen = Rhesus D
Transfusion reactions
- Antigen=ABOsystem

Autoimmune haemolytic anaemia (warm and cold) Immune thrombocytopenia Purpura
Goodpasture’s syndrome

Graves’disease
− Increased thyroid activity − Antigen = TSH receptor
Myastheniagravis
− Impaired neuromuscular signalling − Antigen = Acetylcholine receptor

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

Describe the importance of complement pathways

A

S

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

Describe haemolytic transfusion an example of disease caused by type 2 hypersensitivity by IgM

A

An example of disease caused by type II hypersensitivity (IgM)
Haemolytic transfusion reaction
• Life-threatening condition
• Shock, kidney failure, circulatory collapse, and death

Immune mechanism
• Incompatibility in the ABO or rhesus D antigens
• Donor RBC destroyed by recipient’s immune system
• RBC lysis induced by type II hypersensitivity involving
by the naturally occurring antibodies (IgM)

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

Desribe haemolytic disease of the newborn as an example of disease caused by type 2 hypersensitivity

A

Rh pos father, rh negative mother, first child - rh+ antigens from first fetus go into mothers blood. The mother then produces anti rh antibodies. woman’s body mounts immune response against rh in fetus (second time) - damage fetus rbcs

Rhogam - immunoglobulin - IM - prevent the mother from mounting an immune response against the fetal cells - 72h after deliver

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

What are therapeutic approaches for tissue/cell amage in type 2 hypersensitivity reactions

A 
• Anti-inflammatory drugs - Complement activation
• Plasmapheresis
 Circulating antibodies and
inflammatory mediators
• Splenectomy
- Opsonisation/Phagocytosis
• Intravenous immunoglobulin (IVIG) 
- IgG degradation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What re the therapeutic approaches in physiological change as a result on the 2 reacto

A
  • Correct metabolism
  • Antithyroid drugs in Graves’s disease
  • Replacement therapy
  • Pyridostigmine in Myasthenia gravis - replace neurotransmitter
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is plasmapheresis thepay

A

Can get rd of palms, cytokines, replace with substitution fluid. Short term relief and allows healing of damaged tissue, used in Myasthenia gravis Goodpasture’s syndrome Graves’ disease

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

Gove an overview of type 3 hypersevitiity x

A 
• Usually develops within 3-8 hr
• Involves immune complexes between
IgG or IgM and antigens
• Targets soluble antigens 
- Foreign(Infection)
- Endogenous (self antigens)
• Tissue damage caused by the deposition of immune complexes in host tissues
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are key factors affecting IC pathogeneis

A

Complex size
 Small and large size ICs cleared
 Intermediate size ICs
Rbcs have a receptor for c3b - phagocytes can engulf this as it has been opsonised. I a patient has complement deficient - immune disease

• Host response
 Low affinity antibody
 Complementdeficiency

• Local tissue factors
 Haemodynamic factors
 Physicochemicalfactors

All of the above
Persistence of ICs
Deposition
• Joint
• Kidney
• Small vessels • Skin
Multisystem disease
17
Q

Give an overview of type 3 mechanisms s

A

Ss Tend to deposit - problems start where they deposit - cant bind to receptor start a pathway - c3b can opsonise the tissue - can release chemoattractatt v3a which attracts neutrophils - stick to c3b - signal start degradation, releasing toxic material - tissue damage. Neutrophils are essential in driving the damage

18
Q

Gve 2 example of diseases caused by type 3 reactions

A 
• Rheumatoid arthritis (self-antigen) 
• Antigen = Fc portion of IgG (75%)
• Articular and extra-articular features • Episodes of inflammation/remission
• Poor prognosis factors 
-  <30year-old
- High-titreofRF 
- Female
- DR4allele
- Joint erosions

• Glomerulonephritis (infectious)

  • Bacterial endocarditis
  • Hepatitis B infection
• Systemic lupus erythematosus 
• Antigen = Ds-DNA
• Most prevalent immune complexes
disease
• Ratio female:male (9:1)
• 40-60% patients with cardiac,
respiratory, renal, joint and
neurological features
• Repeated miscarriage
• Every patient is unique!!!!!!
19
Q

Give an overview of type 4 reactions

A
  • Usually develops within 24-72hr
  • Involves lymphocytes and macrophages
  • Different subtypes (clinical outcomes)
  • Contact hypersensitivity
  • Tuberculin hypersensitivity
  • Granulomatous hypersensitivity
20
Q

Give an overview of the pathogeneis of type 4

A

First encounter . APC meets bacteria, activates TH1 - specific against this trigger/TB is a good example. A set of effector cells and memory T cells against (eg) TB, first encounter nothing happens. Re encounter - effector chase where you get damage. Macrophages are reactivated by th cells - recognise the bacteria. Activated th, then activate macrophage, these try to clear microbe (but Tb cannot be cleared). Macrophages release toxins, ROS, etc, but this locally damages the tissue and recruite more th cells then activate cd8 -. Pathway -> tissue damage. Triggers local inflammatory response

21
Q

What are some disease caused y type 4

A 
Contact hypersensitivity 
• Occurs 48-72 hr postexposure
• Epidermal reaction
• Require endogenous proteins
• Examples 
o Nickel (common)
o Poison ivy
o Organic chemicals
Granulomatoushypersensitivity 
• Occurs 21-48 days post-exposure
• Tissue damage 
• Examples:
o Tuberculosis
o Leprosy (tuberculoid) 
o Schistosomiasis
o Sarcoidosis
• Pancreatic Islet cells:
o Insulin-dependent diabetes mellitus
• Thyroid gland:
o Hashimoto’s thyroiditis
• Fc portion of IgG:
o Rheumatoid arthritis
22
Q

Describetype 3 and4 therapy

A 
Anti-inflammatory drugs
• Non-steroidals
• Corticosteroids (oral prednisolone)
• Second drugs as steroid-sparing agents (<10 mg oral steroid)
- Azathioprine
- Mycophenolate mofetil 
- Cyclophosphamide

Monoclonal antibodies
• B Cells and T cells
• Cytokine network
• APCs

Immunology (7 decks)

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