Brainscape's Knowledge GenomeTM

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


See full index

Immunology > Hypersensitivity + Role of Each Ig = important > Flashcards

Hypersensitivity + Role of Each Ig = important Flashcards

1
Q

What is hypersensitivity

A

Group of disorders

Immune system = exaggerated or inappropriate response to environmental antigens which do not usually cause damage

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

What are the types of hypersensitivity

A

Type 1 = allergy
Type 2 = cell / cytotoxic - IgG or IgM binding to antigen
Type 3 = immune complex
Type 4 = delayed / T helper travelling to antigen and relcruiting macrophages
Type 5 = Ab

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

What is type 1

A

Antigen binds to IgE bound to mast cell in blood which triggers release of histamine / other cytokines
Causes immediate allergic reaction or anaphylaxis

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

What causes type 1

A

Genetics - hypersensitive T cells releasing Th2

Environment

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

What is allergy

A

Clinical expression of atopy
Hypersensitivity to allergen that immune system recognises as foreign
Large proportion can be atopic without developing allergy

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

What is atopy / atopic triad

A 
Genetic tendency to develop allergic diseases due to hypersensitivity 
Triad of 
- Asthma
- Eczema
- Hayfever
Also food allergy / allergic rhinitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is pathophysiology behind sensitisation phase of type 1

A

APC picks up allergen
Goes to LN
CD4 predisposed to respond aggressively (atopy)
Release Th2 cytokine + IL
IgE produced by B cells
Bind to mast cell in blood = degranulation on repeat exposure

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

What happens in reaction phase early

A

Allergen binds to IgE
Mast cells immediate degranulate on 2nd exposure
Histamine released = inflammation
Leads to mucosal oedema / secretion / muscle contraction + vaasodilator + increased permeability
Leads to rash, swelling, wheeze, cough

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

What happens in late reaction phase

A

8-12 hours after allergy
Further differentiation of Cd4 and TH2
Other cells - eosinophil / basophil / leukotrienes

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

What are examples of diseases of type 1

A

Atopic dermatitis

Anaphylaxis

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

How do you investigate type 1

A

History - timing, exposure, symptoms, FH
Skin prick
Skin patch testing
Serum tryptase - rises after allergic response
Serum IgE
RAST
Food challenge = best way

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

What is skin prick useful for

A 
Food + pollen allergy 
Inexpensive and easy to perform 
Diluted allergen pierced into skin 
Histamine = +ve 
Sterile water = control 
Wheel forms if allergic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

When is skin patch testing used

A

Contact dermatitis (type IV)

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

What is RAST

A 
Determines amount of IgE reacting to specific allergic
Graded 0 (-ve) to 6 (+ve)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How do you treat type 1 hypersensitivity

A 
Avoidance of allergy 
Anti-histamine
Corticosteroid
IM Adrenaline in anaphylaxis 
May need epipen if serious reaction 
Desensitisation immunotherapy = expensive
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is type 2 hypersensitivity

A

Ab mediated destruction of cells by activating complement
IgG or IgM
Antigen can be self or exogenous so blur between autoimmune + hypersensitive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How does Ab mediated desutrciton

A 
MO / Neurtrophils = phagocytosis 
Complement activation via antigen / Ab complex
MAC forms 
Opsonisation
NK cells = apoptosis 
ADCC
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are clinical disorders of type 2 hypersensitivity

A 
Haemolytic reaction - autoimmune to self or after blood
Haemolytic disease of new born
Hyperacute graft rejection
Transfusion reaction 
Myasthenia graves
Anti-GBM
Pemphigus
ITP
19
Q

How do you treat / prevent

A

X-match
Tissue typing
Rhesus screening
Immune suppression if autoimmune / transplant rejection

20
Q

What is type 3 hypersensitivity

A

Abnormal deposition antigen / antibody complex in tissue

Can be due to self or exogenous antigen

21
Q

Physiological immune complex formation

A 
Plasma cells release IgM to pathogen
Picks up antigen
Presents to T helper via MHC
Creates bond
Releases IL and B cell switching occurs
Activates complement / opsonisation + phagocytosis
22
Q

When does it become hypersensitive

A

If occurs with small molecules that are not normally picked up by MO e.g. DNA
Forms abnormal complex and tissue damage
Symptoms 4-10 hours after exposure
System illness if form in circulation
Localised if form in tissue

23
Q

What is an example

A

SLE
RA
HSP
Failure of tolerance = auto reactive T and B circulate
Anti-dsDNA produced inappropriately
Complex land anywhere so systemic illness

24
Q

What precipitates

A

Infection / sunburn

Damages cells and releases DAN which is detect as foreign

25
Q

How do you Dx

A

Clinical
Biopsy
Immune complex
Ab

26
Q

How do you treat

A

Treat precipitating
Remove complex
Immunosuppression

27
Q

What is type 4 hypersensitivity

A

Involves overactivity of Th1 and Th17 cytokines to APC of exogenous hapten

28
Q

What does it not respond to

A

Intracellular infection / malignancy

29
Q

What does Th1 and Th17 release

A

Il
IFN-y
Encourages complement and inflammation leading to tissue damage

30
Q

What is it similar too

A

Like atopy but no genetic conponent

Takes longer - up to 48 hours

31
Q

What are examples

A

Mantoux test
Organ transplant rejection
Contact dermatitis

32
Q

What happens in contact dermatitis

A

Happens cross stratum corneum of skin = antigen
Langerhan (APC) present to Th1
Release of TNF-a and Il
More aggressive 2n time

33
Q

What stops going to anaphylaxis

A

Adaptive immune system

Always have T regulatory cells to stop

34
Q

How do you Rx

A 
Avoid allergen
Anti-microbial for infection
Anti-inflammatory
Steroid 
Immunosuppression
Monoclonal Ab
35
Q

SUMMARY

A

Type 1 = allergic IgE mediated
Type 2 = cell surface antigen bound to Ab activating complement, opsonin and MO
Type 3 = Ig clump with lysed products to form complex
Type 4 = Th1 cell adaptive response to pathogen taking up to 48 hours

36
Q

What is anaphylaxis

A 
Life threatening severe type 1 allergic reaction 
Urticarial lesions
Itch 
Angio-edema around eyes and lips 
Abdominal pain

Indicative of anaphylaxis = airway comprise
Swelling + oedema of airway = stridor and wheeze
Tachycardia
SOB
Collapse

37
Q

How do you treat

A 
ABCDE
Adrenaline IM anterolateral aspect of mid thigh 
Repeat every 5 minutes
Hydrocortisone IV
Chloroamphetamine IV
Can give salbutamol if wheezing
38
Q

What are doses of hydrocortisone

A

200mg >12
100mg >6-12
50 mg >6 months-6
25mg <6 months

39
Q

What are doses of chloramphetamine

A

10mg >12
5mg 6months-12
2.5mg <6months

40
Q

What can be taken after to prove anaphylaxis

A

Serum tryptase within 6 hours

41
Q

What must you do after an episode of anaphylaxis

A

Observe patient for 6-12 hours incase biphasic reaction occurs
Teach about epipen
Refer to allergic clinic

42
Q

What dose of adrenaline

A

1 in 1000 0.5ml

43
Q

What dose of adrenaline in resus

A

1 in 10,000 10ml IV

Immunology (7 decks)

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